0

The
Journal
of
IiME
Volume 3 Issue 1
from
Invest in ME

Journal of IiME
Volume 3 Issue 1
www.investinme.org
P Prroovviiddiinngg aa vvooiiccee ffoorr tthhoossee sseevveerreellyy aaffffeecctteedd wwii tthh mmyyaallggii cc
e enncceepphhaalloommyyeell ii tt iiss
Invest in ME has published a book which we
hope will help healthcare professionals,
media, ME Support groups and people with
ME in their quest to improve education
regarding Myalgic Encephalomyelitis (ME).
The name ' Lost Voices' refers both to the fact
that people who are severely ill with ME are
generally not in a position to make themselves
heard, and also to the way that
the prejudiced denial of ME - as an 'aberrant
belief' rather than a devastating physical
• It clearly and movingly shows the
evidence of the devastating impact this
physical disease has on individuals and
their carers and families
• It will bring to more public notice the
plight of ME sufferers
• It will help change a widespread lack of
comprehension based on general
misinformation, vague definitions and
manufactured statistics, to the
development of empathy and concern
for those who are so ill
illness - has meant that often others are
incapable of actually hearing and seeing
what is being said and shown.
'Lost Voices' is primarily written by people
affected by severe ME- whether as sufferers,
carers or families.
The book provides the following -
• It allows an opportunity for people who
are usually invisible and unheard to speak
for themselves, so that their situation can
be seen and understood more clearly
Invest in ME (Charity Nr. 1114035)
• It can educate the medical profession, the
public and others such as wider family
• It will, hopefully, encourage a sense of
community among ME sufferers and those
supporting them
The book is an A4 landscape size with a
laminated card cover.
The stories and photographs are provided by
carers, families and, as far as possible, people
with ME themselves. 'Lost Voices' represents
Continued page 3
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Journal of IiME
Volume 3 Issue 1
Lost Voices
A A vviieeww ffrroomm OOll iivveerr ,, wwhhoossee oollddeerr ssiisstteerr hhaass sseevveerree MMEE
"Lost Voices” is not just a book about ME/CFS,
rather it is a book that has been created and
written by the very people who experience
the illness first hand; severe sufferers, their
carers and their families.
The combination of photographs, images and
writing found in Lost Voices beautifully express
the realities of the illness and its impact not
only on the sufferers but on their friends and
families as well, giving a voice to so many
people who have been left to fight this
debilitating illness in isolation.
It does not just tell one person's story or even
one family's story. Lost Voices brings together
and shares the stories of many different
individuals, families, carers and friends; each
story unique, each story providing an insight
into a world that has been invisible to most
people for too long.
Anyone who has suffered from or is still fighting
ME/CFS will find Lost Voices a powerful and
uplifting reminder that they are not alone,
that there are so many others like them,
fighting for recognition, fighting for
understanding and fighting for fair and
effective treatment. This is a book full of love,
courage, hope and determination.
This book is not just for those suffering from
ME/CFS but is also for their carers, friends and
family members. You can share the
experiences of others who have been sucked
into this hidden and isolated world.
It provides an invaluable way of explaining
this illness and its impact to those who are
fortunate enough not to have experienced it
first hand.
Lost Voices contains contributions offering
insight and expertise from leading figures in
the ME/CFS research and support community.
The forward has been written by Leonard
Jason, former Vice President of IACFS/ME: -
'...Lost Voices will help healthcare
professionals and others become less
Invest in ME (Charity Nr. 1114035)
judgmental, and more tolerant and
understanding of those with ME, for these
are the voices of heroes...
there were moments of wonder when I
realized that these patients have something
uniquely profound to share with a world so
saturated with materialism...
these patients are asking us to wake up from
our stupor...
Their courage and life affirming stories
challenge us to act. Just as the Civil Rights
and Women’s movements focused our
attention on serious inequalities and the
need for activism, so does Lost Voices force
us to recognize the needs of children and
adults with ME and to join the fight for a
cure.'
The introduction to Lost Voices is an invaluable
asset for anybody who has ever tried to answer
the question 'What is ME/CFS?' It examines
some key areas of confusion which have
resulted in misconceptions and ignorance
about the nature and severity of the illness
amongst the general public, the government
and the medical profession. Cutting through
this misunderstanding, the introduction to Lost
Voices argues powerfully for a new biomedical
focus on subgroups to drive future ME/CFS
research and treatment.
Lost Voices is a book to help others understand
the hidden reality of life with severe ME; a book
that allows one to feel the comfort of shared
experience whether it be suffering, courage,
love, hope or determination; a book with key
information about ME; a book to be moved by;
a book to enjoy.
Please buy Lost Voices and use it to help fight
the ignorance and injustice that results in so
many ME sufferers struggling invisibly and
unheard.
The purpose of this book is to educate in the
broadest possible sense and it is not being sold
for profit by Invest in ME."
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www.investinme.org

Journal of IiME
Volume 3 Issue 1
www.investinme.org
Conference Edition Editorial Comment
Welcome to the 2009 conference edition of the
Journal of IiME – a blend of science, facts,
stories and news regarding Myalgic
encephalomyelitis (ME or ME/CFS). May is ME
Awareness Month and also the month when
Invest in ME hosts its annual biomedical
research conference. It is an apt time to look
back at what has occurred in the last year as
well as to look forward to future developments.
In the year which has elapsed since our 2008
conference some events have occurred which
will have consequences for people with ME
and their families, for researchers and health
services when it concerns ME. These events are
a mixture of regret, disappointment, anger but
also progress and hope.
The last year has seen the NICE guidelines for
ME being promoted and, some would argue,
forced upon the health services and unwilling
patients.
The dissatisfaction with the NICE guidelines has
seen a patient revolt and NICE, yet again,
being taken before a Judicial Review to
defend its processes and its decisions by the
very patients it was meant to protect and to
treat.
A major criticism of NICE is that it failed to look
at the established, published biomedical
research and instead produced a document
which is neither helpful for patients nor useable
by medical professionals. Its scope, based on
flawed input, was also far too narrow to make
any meaningful difference.
One of the most disappointing aspects of the
Judicial Review was the spectacle of NICE
Disclaimer
The views expressed in this Journal by contributors and others do not necessarily represent those
of Invest in ME. No medical recommendations are given or implied. Patients with any illness are
recommended to consult their personal physician at all times.
attempting to paint these guidelines as a
“gold standard”. This risible self-assessment
by NICE showed a flawed organisation
which needs overhauling.
Another organisation failing people with
ME has been the Medical Research
Council. The last eighteen months has
witnessed the UK Medical Research
Council officially acknowledge that its
previous policy toward ME research has
been an abject failure by setting up a new
panel to look at research into ME.
There is doubt of the genuineness of the
MRC to seriously change its approach. The
criticism which IiME has of this panel is that
it includes some who wish to reclassify, or
who perceive ME as a behavioural illness
and this undermines the reason for this
panel’s existence and its continued
operation.
With its usual tardiness the MRC has spent
eighteen months since the panel’s
inception and has yet to produce
anything of substance. We would suggest
to the MRC that the patient community
might have far greater involvement in this
panel than it currently allows. We also
believe that the eventual decision-making
process of subsequent research proposals
by that panel and any peer reviewers
must be completely transparent –
something the MRC continues to fail to do
and which has seen obvious bias in
funding of research into ME in the past.
The need to sub group ME patients to
allow proper research and treatments was
Invest in ME (Charity Nr. 1114035)
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Journal of IiME
Volume 3 Issue 1
Comment
highlighted at our last conference and from
there we move on this year to focus on severe
ME.
The severely affected are a group of patients
who do not figure often in research – which
may be due to the lack to appropriate
funding.
The severely affected people with ME are
neglected by healthcare organisations and
by the establishment authorities responsible
for funding research. Many believe it is only by
examining severely affected patients that the
true nature of this illness is revealed and
treatments and cures will be found.
Appropriately, to coincide this year with our
emphasis at the conference on severe ME
Invest in ME has published the Lost Voices
book – a unique collection of stories,
photographs and facts which highlights the
effect of severe ME on patients, on families
and on society. Lost Voices has already been
distributed to twenty countries and is to be
found in medical libraries, community libraries,
hospitals, GP surgeries, and a whole raft of
various places within the community.
The IiME International
ME/CFS Conference
London 29tthh May 2009
Since the last Invest in ME international
biomedical research conference the
European ME Alliance (EMEA) has also been
created and meets in London after the
conference for its first AGM. The Alliance now
spans across Europe, the most recent addition
being Spain, and it is hoped to supplement
with the remaining European countries before
long.
The Invest in ME conference in London in May
will be our fourth biomedical research
conference and now welcomes delegates
from four continents and fourteen countries.
We welcome many new delegates as well as
old friends.
Invest in ME (Charity Nr. 1114035)
Some who will not be seen at the conference
(as we go to press) will, again, be the Secretary
of State for Health, the Medical Research
Council and the Chief Medical Officer. Despite
the persistence of IiME in asking, and an
amazing response from the ME community in
petitioning, these main establishment areas still
fail to take ME seriously enough to listen to the
foremost speakers displaying research on their
doorstep.
The sad point about this is that treatments are
available for ME. The IiME 2008 conference
had presentations from Dr John Chia and Dr
Martin Lerner, showing effective treatments for
some sub groups of ME – treatments which NICE
actually refused to endorse.
The fact that treatments by antivirals are
currently expensive is seen as one reason why
they are not used in the UK for ME. Yet the
recent outbreak of swine flu has shown how
easy it is to provide antivirals to anyone
suspected of having contracted this strain of
the flu virus.
Invest in ME have written to the Chief Medical
Officer and asked why is ME any different? Are
lives not worth more than money? Should not
the Chief Medical officer be making a
statement as to why antivirals (or any other
relevant medications) are not used for ME? If
only the CMO would accept one invitation to
the IiME annual biomedical research
conference then he would be able to see first
hand how this might affect real people.
In the absence of progress from the
government, Medical Research Council and
within the NHS we need a CMO who will stand
up for patients.
We need action and leadership and we
cannot afford to lose yet another generation to
this illness.
Perhaps the next year will be different.
IiME will continue with our conferences and are
already putting plans on paper for a bigger
conference in 2010 to celebrate our fifth
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Journal of IiME
Volume 3 Issue 1
Comment
biomedical conference.
So let us take a hypothetical situation which
occurs between our 2009 conference and
leading up to our 2010 conference.
Let us suppose that a diagnostic test was
developed and that sub groups were more
easily able to be identified in order to guide
treatments.
Let us suppose that the disease mechanism
for ME was found?
How would ministers and healthcare officials
react to such changes?
What changes would be seen in the
healthcare system?
How would the pharmaceutical industry react
when there is a promise of great rewards from
development of effective treatments and
possibly cures for ME based on successful
biomedical research?
How would NICE react?
What changes in attitude would come forth
from insurers and Work and Pensions
departments toward the current policies
where benefits are often denied to people
with ME?
Would the CMO change his stance?
Would the Medical Research Council be
more transparent and begin funding
biomedical research based on sound science
rather than on vested interests?
Would the MRC seriously allow funding of
biomedical research to begin?
We believe that researchers such as those at
our conference are making such enormous
progress that we should be looking at the
above scenario and begin to be prepared to
ask these questions.
In the last year we have seen the great
potential of biomedical research being
realised due to the approach adopted by
organisations that have a clear strategy –
amongst them the Whittemore-Peterson
Invest in ME (Charity Nr. 1114035)
We can hope that by our next conference in
2010 the landscape might have changed
significantly enough so that we will be
reporting on progress on this development
and talking of a year of success. For next
year’s conference we hope to be welcoming
more new delegates – including those who
are currently conspicuous by their continuing
absence.
And so to the Journal.
Appropriately, to reflect the emphasis on
severe ME at the conference we have several
articles revolving around severe ME.
Following the death of Alison Hunter from
complications arising from ME the Alison
Hunter Memorial Foundation (AHMF) of
Australia was set up by her mother, Chris. Chris
Hunter has given us permission to republish a
very moving article by Alison – written many
years ago but as relevant today as it was
when Alison wrote it at the age of 17 – a story
which any parent of a child with ME would
Page 7/76
www.investinme.org
Institute. We feel the newly-established
Enterovirus Foundation will also influence the
progress of biomedical research into ME.
Invest in ME has, since its inception, been
advocating a national strategy of biomedical
research into ME as the only logical way
forward. However, this is now being
superseded by the requirement for an
international strategy of biomedical research.
The WPI and the researchers at our
conference are making great strides in
progress and Invest in ME wish to publicise
their work at every opportunity and
encourage people around the world to
support them – both in moral and financial
support.
After the conference Invest in ME will be
working with our European colleagues to
further the establishment of centres similar to
the WPI.
Our Biomedical Research Fund, announced,
in January, will be used to help with this and
provide a focal point for these plans.

Journal of IiME
Volume 3 Issue 1
Comment
today immediately recognise and which
could have come directly from this year’s Lost
Voices book.
How does it feel when a local health
authority fails to provide a biomedical clinical
lead for severe ME patients even though it is
possible? We have the views of one severely ill
patient on this situation.
The story of the Krisner family of Norway was
highlighted on our 2006 conference DVD – a
story of devastating consequences for a
family where three siblings have become ill
with severe ME. Yet there is hope. After
continuing treatment two of the children are
making amazing progress and the other has
made some improvement. Kjersti and Harald
Krisner provide an article showing this progress
– a story of great progress and hope.
The new Enterovirus Foundation has been
created and we welcome members of the
EVF, Professor Steven Tracy and Nora
Chapman, who have provided an excellent
article on Human Enteroviruses and Chronic
Infectious Disease.
Dr John Chia, who is speaking at our
conference, is part of the EVF.
We have two papers from Professor Garth
Nicolson et al – one showing the similarities
between CFS (ME) and Autism Specturm
Disorders and the other discussing weight
issues with CFS (ME) and the use of an all
natural oral supplement mixture.
Epidemics are a less well publicised feature
with ME. Professor Harald Nyland will be
talking about this at the conference yet
epidemics are not new. The Incline village
episode in the eighties is responsible for some
of the foremost ME researchers continuing
their work.
We have an old article on epidemics from Dr
Gordon Parrish which we felt was worthy of
being republished to put the work of today’s
researchers into context.
We also include conference abstracts.
Invest in ME wish to thank those organisations
Invest in ME (Charity Nr. 1114035)
We would like to thank the Irish ME Trust and
the Alison Hunter Memorial Foundation for
their donations, support and friendly
cooperation.
and individuals who have donated or
sponsored to enable us to bring about the 4th
Invest in ME International ME/CFS Conference
2009. Thank you for your generosity.
www.investinme.org
.
To those who attend the conference we
hope you enjoy your day and learn a great
deal. For those not able to come to the
conference then we hope the Journal will
provide something of use. The conference
promises to reflect the real progress which is
finally beginning to benefit people with ME
despite being enacted on a background of
terrible suffering and intransigence of those
responsible for deciding healthcare policy.
Enjoy the Journal, enjoy the conference.
ME FACTS
The US Centres for Disease Control
(CDC) website confirms that:
“The name ME was coined in the
1950s
to clarify well-documented
outbreaks of disease; ME is
accompanied by neurological
and muscular signs
(sic) and has a case definition
distinct from that of CFS(ME)”.
(http://www.cdc.gov/cfs/cme/wb
1032/chapter1/overview.html ).
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Journal of IiME
Volume 3 Issue 1
SEVERE ME –
A PATIENT’S VIEW
Severe ME requires investigation and treatment by biomedical researchers and clinicians
understanding the biomedical basis for the illness.
Against a background of severely affected people with ME facing reluctance from
healthcare authorities to consider their future, then
when a health authority has an opportunity to employ world-renowned researchers and
physicians who understand the illness,
when a patient community is pleading with the same health authority to employ these
same physicians,
then any logical person must ask why isn’t this happening?
Here a long time sufferer of ME has dictated the following article.
I want you to imagine what it is like to have
severe, neurological ME.
I want you to try and think what it must be like
to experience constant ongoing physical
pain, all over your whole body. Pain that
throbs, pain that stings, pain that itches and
irritates, burns and moves, pain that invades
your muscles, your skin, your scalp, your
feet, your eyeballs, your tongue, your
intestines, so that there is no part of you
experiencing any respite from pain, any
second of the day or night, in fact the pain
increases in intensity and agony every time
you try to rest or sleep.
I want you to try and imagine muscle paralysis
that invades you, so that when you awake
you can no longer speak, move your lips
open your mouth, open your eyes, move your
fingers, feel your hands or your arms, your
feet, your toes, your legs.
I want you to imagine what its like to
desperately need to go to the toilet but to be
unable to move, to be unable to sit or stand,
to be unable to walk but worse than this to be
unable to bear to be touched.
So that even if there is someone to move you,
to lift you, to stand you up, to sit you in a
wheelchair, to push you to the bathroom, you
cannot access this help.
Invest in ME (Charity Nr. 1114035)
Day upon day, year upon , year for hours on
end.
I want you to imagine the physical torment of
hyperacusis, of being so hypersensitive to
noise that a whisper sounds like a shout and
that any loud noise feels like a physical assault
not just on your ears and your head but on
your whole body.
I want you to imagine the ordinary things of
life becoming completely inaccessible
because you have no energy, you cannot
breathe easily or fully, you cannot eat so
many different foods because of allergy and
sensitivity, you cannot be in the same room as
people because they drain you of any energy
you might have had and their voices hurt you
and you become more ill if you try to engage
with them.
I want you to imagine a life where the TV hurts
your eyes, where the computer screen hurts
your eyes, the sunlight, even the normal
daylight, without bright sun, hurts your eyes
and gives you severe eye pain.
A head pain that goes on and on for days on
end.
A life where the telephone hurts you to hold it,
to hear it and where your brain is unable to
process any incoming information rendering
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www.investinme.org

Journal of IiME
Volume 3 Issue 1
S SEEVVEERREE MMEE –– AA PPAATT IIEENNTT ’’SS VVIIEEWW
conversation impossible.
I want you to imagine being unable to
read because your brain simply is unable
to comprehend the mass of information
before you; of being unable to imagine,
even, because the fog has descended
inside your head that blanks out thought
and creativity ability.
This is only a portion of the reality of having
severe ME.
Now I want you to think what it must be
like to know that despite this severe
disability, this chronic unending illness:
- There is no biomedical consultant
provided to treat you
- There is no apparent awareness of the
urgent need to do something to
physically help you
- There is no NHS service offering
appropriate biomedical tests or
treatments despite the fact there are
very serious physical
abnormalities in your body and every
time you ask for help you are sidelined
- Every time you try to raise awareness it
doesn't make any difference.
What must it be like then to find that there
is an opportunity for world class,
concerned and interested medical
consultants – consultants who know your
illness is a physical reality, one that has
been grossly neglected, - who actually
want to come and provide a new service,
to right the injustice of no appropriate
medical provision in your area ?
Can you begin to imagine what it feels like
when, instead of this offer being
accepted, you are fobbed off instead
with a biopsychosocial, therapy-led
service (pretending to be biomedical) that
Invest in ME (Charity Nr. 1114035)
does not meet the complex medical needs
of this disease?
When all the PCT has to do is say -
“Yes”,
“we will take you seriously” ,
“We acknowledge responsibility for your
biomedical care”,
“we can see that you need a local
consultant and it is not unreasonable to
expect one;”
“So yes, we will provide you with a new
innovative biomedical service that might
just begin to meet your needs..”
“And we will lead the way.”
Please tell me why this is not happening ?
www.investinme.org
ME FACTS
In 1988, UK researchers Archard
and Bowles et al published the
results of their research into muscle
abnormalities in ME/CFS:
“These data show that enterovirus
RNA is present in skeletal muscle
of some patients with postviral
fatigue syndrome up to 20 years
after onset of disease and suggest
that persistent viral infection has
an aetiological role. These results
provide further evidence that
Coxsackie B virus plays a major
role in ME, either directly or by
triggering immunological
responses which result in abnormal
muscle metabolism”
(JRSM 1988:81:325-331).
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Journal of IiME
Volume 3 Issue 1
Forget M.E. Not
by Alison Hunter
Somewhere in the recesses of my mind there is a
memory of being active, of having the energy to
be active...when sprinting across the street was a
reflex action and a good day was a day in the
surf followed then by dinner at a new restaurant
followed by a movie.
This poignant article is as relevant today as
when it was written by Alison in September
1993. It has been reproduced here by kind
permission of the Alison’s mother Chris
Hunter.
The Alison Hunter Memorial Foundation
The Alison Hunter Foundation was
established in 1998.
The Foundation is an enduring memorial to
Alison Hunter and all those whose lives have
been devastated by ME/CFS.
Alison died in 1996, aged 19, from
complications arising from ME/CFS which
There was a time when my body parts just
existed... now, they ache as if to remind me of
their presence. "Yeah boys, how you doin', still
there, GREAT." An average day now consists of
showering (with a seat), getting dressed, and
perhaps a few hours of study interspersed with
hours on the horizontal.
The fatigue is not everyday tiredness,
experienced after an energetic day's gardening.
It is an exhaustion of body and mind so profound
that it becomes a concerted effort to think, walk
and sometimes even move, sit, eat or breathe.
Arms and legs turn to lead; they sink through the
mattress to eternity...there is often pain
throughout the body which can be constant
and localised (for e.g. continual severe
headache) or migratory...calf muscles one day,
finger joints the next. Then there is nausea,
diarrhoea, ringing in the ears...
Aside from the physical problems there are the
cognitive symptoms (the memory loss, the lack of
concentration) alongside the neurological: the
dizziness and sensitivities to extremes of
temperature, light and noise.
Doctors have at last pinpointed the mechanism
by which such signs occur - lack of blood flow to
Invest in ME (Charity Nr. 1114035)
included seizures, paralysis, gastrointestinal
paresis and overwhelming infection
resembling Behcets Disease.
Such complications are rare and only
present in a severe subgroup.
Alison courageously fought ME/CFS for ten
years and was an unstinting advocate for
young people.
The Alison Hunter Memorial Foundation is a
non-profit institution. The Foundation works
independently in a spirit of support and
cooperation with all researchers, institutions
and ME/CFS societies to advance scientific
knowledge and medical care.
http://www.ahmf.org/
certain areas of the brain. Little comfort when
at the age of 18, one finds oneself unable to
remember one's home address, misspelling or
mispronouncing basic words or walking into a
room with no recollection of why or how.
"How are you?" is a question I'm asked all the
time; every day almost by friends, family. Most
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Journal of IiME
Volume 3 Issue 1
www.investinme.org
Forget M.E. Not (continued)
people don't really want to know; it's a form of
etiquette, and usually a customary "Okay" or
"Not too bad" fits the bill. "Not too good", on the
other hand, or (heaven forbid) "Quite unwell" is
met with a look that says, "Whaddaya mean?!"
I have breached the unwritten code of
greeting...awkward silence ensues.
Admittedly, many don't even listen to the reply:
"How are you?" "Not feeling at all well." "That's
great, did you see the movie on Channel Nine
last night?"
A big problem is that aside from pallor I
generally look healthy enough...a problem,
because one loses credibility when one doesn't
conform to the 'sick stereotype'—supposedly
thin, frail and slow moving—and are
predisposed to comments like "How can YOU
be sick, you don't look at all sick?"
thinking negative certainly doesn't help, but
remarks such as "Chin up", "Look on the
bright side", "There are many people worse
off than you" only serve to alienate. Surely
for a person to be cheerful all the time
given the pain level, lifestyle restrictions etc
would be a cause for concern.
Should these treatments fail it is invariably
because you didn't have the right attitude,
because "Mrs Jones tried it and hasn't
looked back", a mentality accurately
summed up as 'wellness macho'.
We present a challenge to doctors...if they
know us well they believe we are ill but are
at a loss as to how to help...most patients
aren't so lucky and are labelled neurotic,
school phobic, anorexic, menopausal,
hypochondriacal, and are handed a
referral to see friendly Mr — to have a little
chat about why we need to be sick. This is
extremely damaging.
However even the most understanding
doctor becomes frustrated when tests
repeatedly come back 'normal'. They
cannot give us a pill to make it (and us) go
away, and worsening health drives us back
With a disease lacking a diagnostic test
everyone's an expert...everybody knows
someone's niece or cousin twice removed who
went to see Dr So-and-so and now she's
climbing mountains. Each new regime might
be 'the One' to set things moving in the right
direction. They stretch from the sublime to the
ridiculous but you must try them all lest "don't
you ever want to recover?"
These treatments aren't always benign, leaving
you worse off than when you started, not to
mention emotionally and financially.
Seven years down the track there's nothing I
haven't tried: Chinese herbs, positive thinking,
acupuncture, positive thinking, dietary
manipulation, positive thinking, aromatherapy,
positive thinking, electromagnetic therapy, all
the while thinking positive because, "With a
positive attitude you're almost there." Well,
Invest in ME (Charity Nr. 1114035)
again and again in desperation to ask,
"Doctor, can't you do something??"
Rarely will they say, "I don't know what is
wrong with you", which they see as
incompetence, when in fact the patient
already realises this, and is far preferable to
yet another blame-the-patient technique.
For pain, other than strong medication,
distraction therapy wards off insanity in
desperate moments, be it gentle massage,
an engaging comedy, company,
laughter...distraction as a form of pain relief
has been known from centuries such as this
quite probably effective (if outmoded)
example found in the Oxford Concise
Medical Dictionary: "A seton is a skein of
cotton or the like passed below skin and left
with ends protruding to maintain an artificial
issue as a counter irritant."
Page 12/76

Journal of IiME
Volume 3 Issue 1
www.investinme.org
Forget M.E. Not (continued)
Having missed altogether four years of
schooling I may not have received a formal
education, nevertheless I have learnt many
invaluable 'life lessons' I don't believe are to be
found between classroom walls, for example
tolerance, empathy and open-mindedness. I
don't hold much with the enriched sufferer
theories however: "Great, I've suffered
unrelenting pain for seven years, but I'm gonna
be a better citizen."
Books, newspapers, radio and some television
programs...these have been my umbilical cord
to outside life, a world I often don't feel a part
of. I have reached the conclusion that should
be a number one priority although it is
generally taken for granted, even by me; in the
rare instances I catch a glimpse of it, feel the
energy in my fuel tank, I am like a compulsive
spender, spending the last drop plus more until
I am back in bed. In my world you pay for your
fun.
Sometimes it is worth it—often it isn't; we have
no problem with motivation; quite the opposite,
we are our own worst enemies.
My family have been wonderful, after all an
illness like this impacts upon every
member...Mum's had to give up work
temporarily, no more spontaneous family
holidays, siblings take a back seat.
It's hard being a teenager, trying to assert your
individuality while so forcibly dependant on
people for practical care. Of prime importance
to adolescents is the need to feel accepted,
normal, "one of the pack".
This is impossible to achieve when you
mysteriously disappear every day after recess,
receive extensions on assignments and have to
decline invitations to most parties, sporting
activities etc.
I am lucky to have a few "healthy" friends who
are supportive and as understanding as they
can be, who visit when I am bedbound and no
longer ask if I'd like to go on interstate hikes.
I also have strong friendships with adolescents
Invest in ME (Charity Nr. 1114035)
Page 13/76
For years I was going to be "all better next week".
Now I know better, I know the statistics and am
aware that I have moved into the so-called
chronic stage with little chance of spontaneous
remission.
A cure may be just around the corner but I have
to face the fact that I may be sick for a long time
yet.
It's not AIDS, although it's similar, you can feel
equally as ill only it doesn't kill you. Not cancer
either. I'm not dying or anything drastic like that.
It's M.E. Don't forget M.E.
with the same illness—we can provide mutual
support & encouragement...most of all we can
'Lounge Lizard' together.
When you are chronically ill, you tend to lose
your identity to the illness; it defines who you are
and what you are capable of...particularly in
other people's perceptions.
Sometimes I'm tempted to yell, "What about me
the person?" I have thoughts and feelings aside
from those associated with the illness, if not the
opportunity, nor indeed the energy, to express
them.
All the normal adolescent turmoil is experienced,
perhaps magnified and without resolution, for
how do we assert our individuality if not through
experiencing life and interacting with a wide
variety of human beings...certainly not lying in
bed, doing the rounds of specialists once again,
just in case, just to make sure they didn't miss
something "fixable".

Journal of IiME
Volume 3 Issue 1
www.investinme.org
Similarities of ME/Chronic Fatigue Syndrome (ME/CFS) and Autism
Spectrum Disorders (ASD): Comparisons of Co-Infections
(continued)
INTRODUCTION
Although no single underlying cause has
been established for CFS, there is growing
awareness that CFS can have an infectious
nature that is either causative for the illness,
a cofactor for the illness or appears as an
opportunistic infection(s) that aggravate
patient morbidity (1, 2). There are several
reasons for this, including the nonrandom or
clustered appearance of CFS, sometimes in
immediate family members (2-4), the
presence of certain signs and symptoms
associated with infection, the often cyclic
course of the illness and its response to antimicrobial
therapies (2, 5, 6).
Previously we found that Gulf War veterans
with CFS-like illnesses and a positive test for
Mycoplasma fermentans transmitted their
infections to their spouses and children (4).
The adults in these families were diagnosed
with CFS (7) but the children were
subsequently diagnosed with Autism
Spectrum Disorders (ASD) (8). The criteria for
diagnosis of ASD are, in general terms, the
presence of a triad of impairments in social
interaction, communication and
imagination (9).
Examination of ASD patients in civilian
families for the presence of Mycoplasma
species infections revealed that the majority
of these patients had one or more infections
(10).
In ASD cases there are reports of nonspecific
signs and symptoms similar to those seen in
CFS, such as fatigue, headaches,
gastrointestinal and vision problems and
occasional intermittent low-grade fevers
and other signs and symptoms that are
generally excluded in the diagnosis of ASD.
These suggested to some authors that a
subset of ASD patients may suffer from
bacterial or viral infections (11). Here we
examined three commonly found systemic
infections in CFS patients, Mycoplasma
species, Chlamydia pneumoniae and HHV-6
(12-14) and compared the incidence to the
same infections found in ASD patients (10).
Invest in ME (Charity Nr. 1114035)
MATERIALS AND METHODS
Patients: All CFS patients (North American,
n=100) underwent a medical history,
completed a sign/symptom illness survey,
had routine laboratory tests and met the
Fukuda et al. (15) exclusionary criteria.
Control subjects (n=100) had to be free of
disease for at least three months prior to
data collection, and they had to be free of
antibiotic treatment for three months prior
to blood collection. All ASD patients (N=48)
were randomly recruited from patient
support groups in California after diagnosis
of ASD according to the International
Classification of Diseases (ICD-10) and the
Diagnostic and Statistical Manual of Mental
Disorders (DSM-IV). All ASD patients were
assessed by the Autism Diagnostic
Interview-Revised (ADI-R)
(16) and
Childhood Autism Rating Scale (CARS) (17,
18). Most (45/48) had a diagnosis of autism,
while 6/48 were diagnosed with ADD (three
of which were also diagnosed with autism)
and nine autism patients with Asperger’s
Syndrome.
PCR Analysis of Blood:
Blood was collected in EDTA-containing
tubes and immediately brought to ice bath
temperature as described previously (1214).
Samples were shipped with wet ice by
overnight air courier to the Institute for
Molecular Medicine for analysis.
All blood samples were blinded. Whole
blood (50 µl) was used for preparation of
DNA using Chelex (Biorad, Hercules, USA).
Aliquots from the centrifuged samples were
used immediately for Polymerase Chain
Reaction (PCR) as described previously (1214).
Statistics:
Subjects’
demographic characteristics were
assessed using descriptive statistics and
students’ t-tests (independent samples test,
t-test for equality of means, 2-tailed). The
95% confidence interval was chosen for
Page 15/76

Journal of IiME
Volume 3 Issue 1
www.investinme.org
A A RReesseeaarrcchheerr ’’ss VViieeww ff rroomm tthhee WWhhii tt tteemmoorree--PPeetteerrssoonn IInnsstt ii ttuuttee
I was originally exposed to the world of CFS
research, while taking a class in Biostatistics,
as an undergraduate.
My professor was a patient of Dr. Daniel
Peterson and she approached him with the
idea to conduct a research project using his
CFS patient data, to which he agreed.
Although the semester ended prior to
completing the work I continued with the
project on my own and ultimately we
determined the value of CD4/CD8 ratios in
diagnosing CFS and published and presented
these data at the meeting of the American
Mathematics Society in Eugene Oregon.
It was during this time that I became
acquainted with several CFS patients and
truly understood their frustration regarding the
lack of quality CFS research.
I continued to work with Dr. Peterson on an
informal level conducting other research but
eventually I left the Tahoe area and began
my Graduate work at Temple University.
After a short time on the East Coast things
took me in a different direction and I found
myself back in Nevada. Shortly after returning
I entered Graduate school at the University of
Nevada, Reno and that is where I concluded
my Graduate work, receiving a Ph.D. in
Biochemistry in 2006.
Although my Graduate work was conducted
in Neuropeptide chemistry, I never lost
contact with the CFS community and my
desire to help the patients drew me back into
the field; to this day I continue the work that
started many years ago in the medical office
of Incline Village.
Although there are many directions a new
investigator can take when he or she decides
what area of research to pursue, ultimately,
my decision was most greatly influenced by
the CFS patients I met in Dr. Peterson’s office.
I often imagined what it must be like to have
a disease where the cause is unknown, the
treatment is dubious and the mainstream
medical community questions the validity of
your disease.
With this thought in mind it was an easy
decision to continue down the path of CFS
Invest in ME (Charity Nr. 1114035)
Dr. Vincent Lombardi
Dr. Lombardi was introduced to the
field of ME/CFS as an undergraduate
research assistant for Dr. Daniel L.
Peterson, in Incline Village, NV.
While working with Dr. Peterson, he
was responsible for routine
laboratory work, patient interviews,
statistical and epidemiological data
analysis. He began his graduate
studies in the laboratory of Dr. Robert
Suhadolnik at Temple University in
1999 studying the role of RNase L
dysfunction in ME/CFS. He finished
his graduate work at the University of
Nevada, Reno in the field of neuropeptides
and protein chemistry,
receiving his PhD in Biochemistry in
2006.
research, even thought the path is not
always so easy.
I have never been the kind of person
that takes the easy road but the patients
appreciate my work and that is enough
for me.
Invest in ME have a page of ways to
help support the ME community,
including the WPI in its important
work.
http://www.investinme.org/helpus.htm#
Donate-to-the-WPI
Page 21/76

Journal of IiME
Volume 3 Issue 1
www.investinme.org
EDUCATIONAL MATERIAL from IiME
I INNTTEERRNNAATTIIOONNAALL MMEE//CCFFSS CCoonnffeerreennccee DDVVDDss
Invest in ME have available the full presentations from the International ME/CFS Conferences in
London of 2008, 2007 and 2006.
These professionally filmed and authored DVD sets each consist of four discs, in Dolby stereo and
in PAL (European) or NTSC (USA/Canada) format. Containing over 6 hours (2008 DVD set), 9 ½
hours (2007 DVD set) and 6 hours (2006 DVD set) – with all presentations plus interviews with ME
presenters and news stories from TV programmes.
These DVDs have been sold in over 20 countries and are now available as an educational tools –
useful for healthcare staff, researchers, scientists, educational specialists, media, ME support
groups and people with ME and their carers/parents. Full details can be found at -
http://www.investinme.org/InfoCentre%20Education%20Homepage.htm or via emailing Invest
in ME at meconference@investinme.org.
Price £14 each - including postage and packaging.
Canadian Guidelines
Invest in ME are the UK distributors for the Canadian
Guidelines. Described even by NICE as “the most
stringent” guidelines available these are proper, upto-date
clinical guidelines which can also be used as
a base for research criteria.
Findings from the study by Leonard A. Jason PhD
(Comparing the Fukuda et al. Criteria and the
Canadian Case Definition for Chronic Fatigue
Syndrome) indicated that the Canadian criteria
captured many of the cardiopulmonary and
neurological abnormalities, which were not currently
assessed by the Fukuda criteria. The Canadian
criteria also selected cases with ‘less psychiatric comorbidity,
more physical functional impairment, and
more fatigue/weakness, neuropsychiatric, and
neurological symptoms’ and individuals selected by
these criteria were significantly different from
psychiatric controls with CFS.
The Canadian Guidelines provide an internationally
accepted means for clearly diagnosing ME The
Canadian Guidelines are available from IiME and
the price is 80p per copy plus postage & packaging.
To order please contact Invest in ME via this email
address: info@investinme.org
Invest in ME (Charity Nr. 1114035)
Page 22/76

Journal of IiME
Volume 3 Issue 1
Human Enteroviruses
and
Chronic Infectious Disease
Steven Tracy1 and Nora M.Chapman2
Enterovirus Research Laboratory, Department of Pathology and Microbiology,
University of Nebraska Medical Center, 986495 Nebraska Medical Center, Omaha, NE
68198-6495, USA.
1, stracy@unmc.edu 2, nchapman@unmc.edu
ABSTRACT
Most of what is known about human enteroviruses
(HEV) has been derived from the study of the
polioviruses, the HEV responsible for poliomyelitis. The
HEV are generally not thought to persist for long
periods in the host: an acute, sometimes nasty,
infection is rapidly eradicated by the host's serotypespecific
adaptive immune response.
Our discovery that the commonly encountered HEV,
the group B coxsackieviruses (CVB), can naturally
delete sequence from the 5' end of the RNA genome
and that this deletional mechanism results in long-term
viral persistence, in the face of the adaptive immune
response, has substantially altered this view.
This previously unknown and unsuspected aspect of
enterovirus replication provides an explanation for
previous reports of enteroviral RNA detected in
diseased tissue in the apparent absence of infectious
virus particles.
Introduction
The enteroviruses are an incredibly diverse and large
genus in the family Picornaviridae. Within the
enteroviruses, human enteroviruses (HEV; those which
infect humans as opposed to other species) number
at least 100 known serotypes, with more known to exist
but which have just not been characterized to date.
Serotype defines the virus: it is how the immune system
recognizes the complex aggregation of proteins
which makes up the virus particle or virion.
Thus, infection with one HEV serotype induces
immunity that protects against disease which that HEV
serotype might inflict upon one were the virus is
encountered again, but this protective immunity does
not extend to other serotypes. This is why the poliovirus
vaccines work to protect from poliomyelitis: any
Invest in ME (Charity Nr. 1114035)
Page 23/76
Professor Steven Tracy
Ph.D.
Department of Pathology
and Microbiology, University
of Nebraska Medical Center,
Omaha NE 68198-6495;
stracy@unmc.edu; 402-5597747
•
Ph.D., 1979, Department of
Biology, University of
California, San Diego
• Primary research interest:
Molecular biology and
pathogenesis of the group
B coxsackieviruses since
the early 1980s
www.investinme.org

Journal of IiME
Volume 3 Issue 1
www.investinme.org
Human enteroviruses and chronic infectious disease (continued)
subsequent infection with poliovirus is quickly
suppressed by the pre-existing anti-poliovirus
immunity and the virus infection eradicated.
But of course, anti-poliovirus protective
immunity does not protect from being
infected with a different HEV.
Human enterovirus virions are small at 29nm
in diameter; said another way, this means
about 345,000 viruses would need to be lined
up to equal one centimeter. The virus
particle consists of an ordered array of 4
capsid proteins that forms an icosahedral
structure of incredible beauty. In Figure 1, the
reader can see what the coxsackievirus B3
(CVB3) virion would look like were one able to
actually see it. This structure was solved with
a technique called X-ray crystallography(23)
in which X-rays, which are directed through
crystals of virus and bent in specific ways, are
then interpreted by computer analysis to
provide a virus structure. Numerous other
images of related enteroviruses can be found
by visiting the website of the Institute for
Molecular Virology at the University of
Wisconsin in Madison WI, USA.
The HEV cause a plethora of different human
diseases and syndromes, the most important
of which are poliomyelitis [now largely,
although not entirely, eradicated in the world
through use of the vaccines(16)], meningitis
and encephalitis, myocarditis, pancreatitis,
myositis, and type 1 (insulin dependent)
diabetes (T1D)(31).
Recent work has also indicated a possible
role for HEV in the poorly understood etiology
of chronic fatigue syndrome (CFS)(9, 11).
Polio, T1D and CFS are noteworthy, in that
these diseases are chronic and in the case of
polio and T1D, fatal without treatment.
Certainly, fatal cases of the other HEV
diseases occur as well(28) but as a rule, HEV
diseases are deemed to be acute illnesses of
relatively low clinical importance because
they are so common. Nonetheless, 5-10
million cases of symptomatic HEV infections
occur annually in the US alone(27).
Group B coxsackievirus infection of the heart
Within only a few years after their discovery in
Invest in ME (Charity Nr. 1114035)
the late 1940s, the group B coxsackieviruses
(CVB) were shown to be involved in
inflammatory heart disease or
myocarditis(6, 12, 32). Because of the ease
with which the CVB replicated in mice, an
experimental model to study myocarditis
was soon available and has been exploited
for numerous studies over the years.
Once myocardial biopsy techniques
became widespread as a clinical assay for
the presence of myocarditis(29),
researchers became interested in
determining how often HEV was associated
with myocarditis. These studies have
demonstrated that about 15-20% of adult
myocarditis cases can be associated with
an HEV infection(2). This was carried out in
most cases by isolating RNA from very small
biopsy samples of the human heart, then
analyzing the RNA for the presence of HEV
RNA using a variety of techniques.
Interestingly, in those adult cases of
myocarditis in which the presence of virus
was shown by detecting the viral RNA,
rarely can an infectious virus be isolated.
This is confusing: how can one detect viral
RNA and not detect the virus? And indeed,
this was a conundrum for many years. Most
HEV cause cells in culture to die; this
outcome, termed cytopathic effect or cpe,
is the result of the virus infecting the cells in
culture and killing them in the process of
producing the next virus generation. Failure
to observe cpe upon inoculating cell
cultures with homogenized heart samples,
was taken to be evidence that virus qua
virus was not present. This goes back to the
foregoing discussion, in which the general
view of HEV is as a virus that rapidly causes
cell lysis (acute disease). As opposed to
adult samples, samples of pediatric
myocarditic heart tissue generally shows
both the presence of cytopathic virus when
placed in culture as well as the presence of
viral RNA when molecular assays are carried
out.
We considered the possibility that HEV
infections of adult human hearts might
generate a population of viruses that have
been characterized and termed defective
interfering (DI) viruses(10, 13). Although DI
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Human enteroviruses and chronic infectious disease (continued)
HEV had never been demonstrated in
humans or animals, they had been shown to
exist in experimental cell culture and thus,
the possibility that they might also exist in
nature could not be excluded. Defective
interfering HEV are viral RNA genomes that
have deleted variable parts of the
sequence that encode the capsid (coat)
proteins of the virus (see Figure 2). This
implies such viruses could never be
successful, as they could never produce an
intact virion. However, DI HEV exist in a
dynamic equilibrium with so-called wild type
HEV which do produce normal capsids.
Therefore, the DI viruses are parasites upon
the wild type population of HEV, using their
capsids to package the mutated RNA for
movement to the next cell. Using a mouse
model of CVB3-induced myocarditis, in
which viral RNA was detectable in the heart
tissue for many days after cytopathic virus
was no longer detectable in cell culture, we
searched for evidence of DI forms of CVB3
RNA but were repeatedly unsuccessful.
We decided to examine the entire viral
RNA genome that was present in these
mouse heart samples, asking the basic
question: are there deletions anywhere else
that might explain this odd phenomenon?
When this was done, we discovered that
one of the ends of the single strand of RNA
that makes up the viral genome, was
missing: these viral genomes were then
called 'terminally deleted' or TD(8, 18, 19).
What makes this discovery fascinating to
virologists, is that the sequence which the
virus naturally deletes, was hitherto thought
to be absolutely essential for virus
replication. Our results, however, showed
that while this sequence was very important
for efficient CVB replication, it could
nonetheless be done away with, and yet
have the virus survive.
The cost of this survival is, however,
extremely slow replication. A further cost is
that this survival can occur only in cell
populations that do not divide anymore or
divide very infrequently as in muscle tissue.
It is this reason why we were able to find
these novel virus populations in heart muscle
Invest in ME (Charity Nr. 1114035)
of experimentally inoculated mice(19) and
later, in human heart(8). There are some cell
cultures that do not divide continually but
stop dividing when the cells contact each
other; only in such cultures can CVB-TD
populations occur(18). This is very different
than current cell culture models for
enterovirus infections in which most aspects
of the viral biology are examined in immortal
continuously replicating cells. While this is a
good model for the short term infection of
the gastrointestinal tract in which the virus
infects, rapidly produces progreny virus and
is excreted to infect another individual
before the immune response can curtail
infection, much of the pathology associated
with enterovirus infections is in other
differentiated tissues in which relatively little
cell turnover may occur.
In these nonreplicating
(or only intermittently replicating)
cells, the wild type virus is at a disadvantage
because these cells lack key cytoplasmic
factors essential for rapid replication.
However, the low level replication of the TD
viruses is favored in these cells and as the
intracellular portion of the virus replication
cycle is much longer, it is relatively hidden to
the immune system. Much of our current
research focus is upon the mechanism of
selection of the TD populations in such cell
cultures or tissues.
These results provided an answer to the
conundrum of failing to find cytopathic virus
in myocarditic heart samples despite the
ability to find viral RNA.
Indeed, virus (in TD
form) does exist in such samples but
because the TD populations replicate so
slowly and produce so little virus, they are
difficult to detect. However, because the
defect is not in a part of the viral genome
that makes viral proteins, they do make all
the viral proteins and even virus particles.
But what does the finding of TD genomes
mean for HEV disease?
Chronic disease associated with HEV
infections
The previous discussion has demonstrated
that HEV can persist for longer periods of
time in the immunologically-normal host
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Volume 3 Issue 1
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Human enteroviruses and chronic infectious disease (continued)
than ever had been suspected but that this
came at a price to the virus: very slow
replication and relatively very few infectious
particles produced. In cases of chronic
inflammatory heart disease (chronic
myocarditis) or what is often thought to be a
sequela of this condition, called dilated
cardiomyopathy (DCM), HEV RNA has been
detected in the apparent absence of
cytopathic virus(4, 7, 21). We can now say
with some certainty that in such cases, HEVTD
populations were present.
In DCM, the
heart is failing due to damage to the
Invest in ME (Charity Nr. 1114035)
cardiomyocytes (muscle cells of the
heart). Others have shown that a HEV
enzyme that works on and reduces
proteins, called a protease, can damage
an important cardiomyocyte protein
called dystrophin(3) and that in a mouse
model of this disease(33), dystrophin is
cleaved despite the inability of the virus to
produce infectious particles and this leads
to DCM in the mouse, a scenario that is
closely similar to the low level production
of virus particles by TD virus populations.
Therefore, in this chronic HEV-induced
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Volume 3 Issue 1
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Human enteroviruses and chronic infectious disease (continued)
disease, the long-term persistence of a
slowly replicating HEV can lead to cell
damage, due to the virus' own enzymes it
uses to replicate, and this damage
eventually impacts the function of the organ
(the heart) itself.
Another chronic disease that is closely
linked to HEV infections is type 1 (insulin
dependent) diabetes (or T1D)(15, 30). Type
1 diabetes occurs due to an inability to
control glucose metabolism which is an
outcome from the loss of insulin-producing
beta cells in the pancreatic Islets of
Langerhans(17). Although some cases are
thought to be due only to a specific
expression of individual genetic traits, most
T1D cases cannot be so easily explained
and therefore, environmental factors (like
infections) have been sought to explain how
T1D is initiated(1, 20). One environmental
factor that is high on any list, are the HEV:
many clinical observations and
experimental studies implicate HEV as
agents that can and do trigger T1D onset in
humans(15, 30). While CVB have been
associated with T1D cases, other non-CVB
HEV have also been implicated in T1D onset,
further adding to the evidence for a role of
HEV in T1D onset. At present, it is unclear
whether the HEV involved persists in the host
after the initial infection that sets the disease
in motion, or whether it is more of a classical
HEV acute infection, one that is rapidly
cleared by the immune response. What is
very clear, however, is that CVB can rapidly
trigger T1D onset in a T1D-prone mouse
called the NOD mouse if the mouse is
already prediabetic from its own
autoimmune attack on its pancreatic
islets(14). This means that under certain
circumstances (when one has autoimmune
insulitis present, and one is infected with an
HEV against which one has no pre-existing
protective immunity, and it is the correct
HEV at the right dose), T1D in humans could
likely be initiated by an HEV infection. Using
the rapid onset model in mice to make
inferences for humans, we would predict an
HEV infection that rapidly kills enough beta
cells will initiate T1D. However, the virus
infection might not accomplish this: the virus
might instead kill insufficient numbers of beta
Invest in ME (Charity Nr. 1114035)
cells for T1D to ensue. What then? This is
where the autoimmune (in which one's
immune system attacks oneself) aspect of
T1D sets this disease apart from the
previously discussed chronic heart disease.
In T1D, enough insulin-producing beta cells
must be destroyed in order for T1D to occur:
this can happen by autoimmune processes,
by virus attack, or both occurring together.
We are currently assessing whether longterm
persistence of HEV is a factor in both
the NOD mouse model of T1D and in
human beings.
Chronic fatigue syndrome and the link to
HEV infection
In a paper that received much notice,
Chia and Chia showed that HEV RNA and
protein were detectable in the great
majority of stomach biopsy tissue samples
from patients diagnosed with chronic
fatigue syndrome (CFS) but only in few
biopsy samples from control patients
without the disease(9). This report has
suggested that a commonly circulating
human virus group might be a primary
etiologic agent involved in CFS, a disease
that is marked by a difficult diagnosis and a
near complete lack of understanding about
what agent(s)/mechanism(s) trigger the
disease.
As we have seen from the previous
discussion, HEV may be able to initiate a
disease process just from an acute
infection, which is then resolved, or from a
continuing infection as well, involving a
persistent virus population. Persistence is,
however, a relative term.
In an
immunologically-normal individual, i.e., one
who is able to mount normal vigorous
immune responses against infectious
agents, an HEV infection may be able to
persist via a TD genome mechanism for
some weeks, perhaps months, but
eventually will be eradicated by the
immune response. Thus, such infections are
temporary (unlike herpesviruses or HIV).
Although HEV are common viruses, the very
high positive correlation with the CFS
stomach samples was surprising. In other
known associations of HEV with human
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Human enteroviruses and chronic infectious disease (continued)
diseases, such high correlations have not
been observed. Poliovirus caused paralytic
disease during epidemics(22) but only about
1 out of every 100-200 infections involved
life-threatening paralysis. The HEV, thought
to be primarily CVB, which have been
closely linked to causing myocarditis, have
been detected in about 15-20% of samples
in a variety of studies(21).
To explain the high number of positive
stomach samples with CFS, one must
consider the possibility of a continuing
process in CFS patients of new infections
with different HEV serotypes and/or a
significant number of persistent infections in
the stomach. The difficulty these workers
had in culturing the viruses from stomach
tissue, would be consistent with either HEV
strains that do not replicate well in standard
tissue culture systems and/or the viruses exist
in a form that is difficult to detect. While
most HEV do replicate in certain cell
cultures, others require the use of suckling
mice(27).
It is interesting to consider that a
HEV-TD population would fit such a
description of a 'difficult to culture virus".
At present, these findings are highly
intriguing but need also to be considered
with the proverbial 'grain of salt'. It is of the
highest and immediate importance to
identify the HEV in these stomach biopsies in
order to verify and move forward the theory
that HEV are involved in the CFS etiology.
Are they a specific serotype of HEV or are
they many different types?
This can be determined without culturing
the viruses, by amplification of specific
genome regions and determination of the
RNA sequence(5, 24-26). Once established
which specific HEV are present, relevant
model systems might be developed using
cell cultures and possibly mice, to study the
CFS disease onset process.
Summary
Basic research into the biology of the HEV
has lead to truly fantastic discoveries which
Invest in ME (Charity Nr. 1114035)
in turn, have lead to 'bench to bedside'
advances. Understanding how to culture
animal cells in the laboratory, made
possible propagation of the agent that
causes polio and subsequent studies in
primates, work that in turn lead to the
development of the successful poliovirus
vaccines from which we have all profited.
A search for other viral agents that induce
polio-like disease lead to the discovery of
the coxsackieviruses and indeed many
other HEV.
The development of a mouse to study
retinal disease produced the NOD mouse, a
highly useful mouse strain that is regularly
used in studies of T1D. We know that
serendipity and planning go hand in hand
and often in the laboratory, are hard to tell
where one begins and the other leaves off.
As scientists who focus on all things
enteroviral, we are especially interested in
the findings of Chia and Chia that suggest
the potential for an HEV link in CFS etiology.
Our finding that a deletion in the terminal
portion of the CVB genome, was the
mechanism by which HEV can persist, could
not have been predicted based on what
was known. This finding has opened a
completely new and quite unsuspected
chapter in the very well thumbed volume
on enterovirus biology.
This was elegantly enunciated by Louis
Pasteur in his famous quotation: "Where
observation is concerned, chance favors
the prepared mind." Without the existence
of basic science, most of what we know
take for granted in medicine would not
exist.
It is of the greatest importance to keep in
mind the goal toward which one works in
science, but it is also of equal importance
to simply explore and define the 'new' while
keeping that mind well prepared for finding
new treasures.
It is only through such efforts that we
believe the etiology of CFS will be finally
illuminated.
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Journal of IiME
Volume 3 Issue 1
www.investinme.org
SEVERE ME – A NORWEGIAN EXPERIENCE
H Haarraalldd aanndd KKjjeerr ss tt ii KKrr ii ssnneerr
The Krisner family from Norway whom we
intoduced on the Conference 2006 DVD in a TV
programme (available from the Invest in ME
web site) and in a follow up article has since
experienced considerable changes.
Katrrine, who has been ill since 1999, has
become miraculously better in the past year. In
2003 she woke up from a coma like condition
only to become seriously ill again in 2006. At
that time she was left bedbound for 2 more
years in total darkness, being tube fed and
without any ability to communicate at all.
Her condition was plagued with severe
symptoms, and we fought to keep her alive.
In December 2007 she was prescribed broad
spectrum antibiotics due to an infection. After 2
½ months on this medication, she suddenly
responded in February last year.
She started to speak slowly.
Light and sound sensitivities became a little bit
better also.
She told afterwards how she had gradually felt
getting better, but had no means of
communicating it.
After further blood tests we carried on with the
treatment, but now with three different
antibiotics at the same time. After two more
months, at times with debilitating side effects,
Invest in ME (Charity Nr. 1114035)
The Krisner Family and ME in
Norway
In 2006 we were introduced to the Krisner
family from Norway whose three children
were severely ill with ME.
All three siblings Frode, Katrine and Bjørnar
lived normal lives before their sickness.
Bjørnar was a journalist and TV presenter.
In 2006 they agreed to appear on a
Norwegian TV programme to highlight the
plight of severely ill ME patients.
Doctors could not explain why all three
siblings had the illness. They did not know
whether it was genetic or if there were other
factors which forced three young people to
live several years in the darkness and
confined to bed.
At the time of the program the three siblings
were 29, 26 and 20 years old. Frode
became sick when he was 7 years old,
Katrine when she was 20 and Bjørnar
became really sick when he was 26.
No one could predict if the siblings would
ever get better nor say what can be done to
return them to a normal life.
Page 32/76

Journal of IiME
Volume 3 Issue 1
www.investinme.org
SEVERE ME – A NORWEGIAN EXPERIENCE
everything moved foward quickly, and on the
10th of May 2008 she was in the sitting room for
the first time in two years.
A couple of weeks later she could venture out
into the garden for the first time in seven years.
At this point she was able to be without
sunglasses indoors, but outside sunglasses were
still needed.
The improvement this time is completely
different from the one in 2003-2006. It is so in
every aspect.
The change in May was enourmous, almost
miraculous.
We saw the illness losing its hold, whilst with the
previous period of improvement it was a
constant battle against something
overpowering.
Since June last year Katrine has been a patient
of Professor Kenny De Meirleir.
One tries to remove causes successively and
build up the immune system. The treatment,
change of seasons, infections, continuing illness
and other things, cause the condition to
fluctuate.
She has since May 10th last year, been up
every day and this is something of an
experience for us around her.
She is engaging, reflectful, caring with lots to
give and convey, hungry for information and
knowledge, is realistic in relation to the illness
and at the same time plans for the future.
She still has to be careful and take it easy.
Experience tells us, also this time, that going
too fast brings relapses or, at the very least,
slower recovery.
Her younger brother, Frode, who is 23 years old
and has been ill since he was 7, also
experienced great improvement last year after
several months on a similar treatment protocol
as Katrine.
He had an experience of living with an
’abundance of energy’ for the first time which
was a fantastic experience for him.
To be free from looking for a chair to sit down
on, to avoid detailed planning and giving up a
lot the following days if he was out with friends
the evening before, to be able to live more like
everybody else on good days, became a
Invest in ME (Charity Nr. 1114035)
great experience.
The previous summer was a summer when he
could do more and he and his best friend, who
has been fantastically supportive all these
years, went to south of France for a holiday .
Being such car enthusiasts, they could both
experience many things they had dreamt of in
the past years.
Frode has gradually built up his IT company. He
still has to live a restricted life, but he has a far
greater capacity than before.
Bjørnar, the eldest in the family, now 32 years
old, was the one who was the main character
in the 2006 film when he was interviewed in the
dark.
The TV programme gave the severely ill a face
and set in motion a lot of emotions and
engagement.
The fact that he was a TV journalist with an
exciting career and ended up as a patient
needing care, made an impact on many of his
colleagues. The effort of being on TV such as
having a hair cut and shave, took a lot of
energy out of him and led to further
deterioration of which he still has not
recovered.
At present Bjørnar can communicate with signs
and speak a little if needed or when he has
more energy. If he speaks more than his energy
levels allow, it leads to increasing symptoms
which in turn can be the start of long term
worsening of his condition.
This balancing of trying to avoid worsening of
the condition, is important in moving the
condition in the right direction.
Last year in the spring he was put on a similar
treatment as his siblings but there was no big
breakthrough.
Four months ago it looked like his condition was
finally on its way to improving. At that time his
test samples that were sent to a specialist
laboratory were found to be positive for an
African amoeba. After a few days on a strong
amoeba treatment protocol, he experienced
a radical change in his abdominal pain,
hunger and bowel movement function. He is
still under treatment for many other things that
were found. He feels he is getting gradually
better.
Page 33/76

Journal of IiME
Volume 3 Issue 1
www.investinme.org
SEVERE ME – A NORWEGIAN EXPERIENCE
All three siblings have since June last year
been undergoing treatement under the
guidance of Professor Kenny De Meirleir.
He came along after the extra blood tests
that led to treatment had been done. His
findings fit in with those performed earlier.
It is fantastic to experience improvement
and great to see two of our children come
back to life. We hope that we shall
experience Bjørnar coming out into daylight
in a short while.
Life is exciting.
To be continued next year.
Harald and Kjersti Krisner, parents ( May
2009)
ME STORY
The following day the psychologist came to
give me the results, his words were these:
"If you are to be believed, and your
answers truthful, then you have the mental
age of a senile 71 year old, and I should
section you immediately!
Now if you would truthfully like to tell me
what personal experience led to your M.E.
then I might be able to help you! What
devastating event led to this mental
problem, what made you so depressed?"
I was appalled at this approach to my
illness!! I told him in no uncertain terms that
there had been no devastating event, that
I had not been depressed, that actually my
life for the previous couple of years had
been remarkably uneventful but extremely
happy.
He continued to insinuate that something
must have happened and that I was
obviously depressed - so I pointed out to
him that the only event had been me
becoming ill and that any depression I had
was a result of that!
He then told me he would recommend
that I be placed in another hospital to have
further psychological review because I was
obviously not trying and was actually
deliberately acting ill to gain attention!
- Debbie
Katrine (above) – a photograph taken
on her 30th birthday in May 2009.
ME STORY
In 2004 I caught a kind of flu with an infection of the gut and I never recovered.
I needed 3 years for a diagnosis.
It was a infernal trip into the jungle of the German health care system.
At the onset there was a kind of outbreak in my workplace.
The whole staff had been affected by ME-symptoms.
In 2007 Prof. Dr. de Meirleir in Belgium attested me: This patient suffers from ME/CFS (WHO
93.3).
- Roland
Invest in ME (Charity Nr. 1114035)
Page 34/76

Journal of IiME
Volume 3 Issue 1
www.investinme.org
Call to Action
Why I Support Invest in ME
Like a lot of people, I had no real knowledge
about M.E (Myalgic Encephalomyelitis). I
just assumed it was some luxury illness or 'yuppie
flu', because that is the way the media, especially
newspapers had portrayed this disease.
Then my sister Sophia developed severe M.E. and
two years into her suffering, it began to dawn on
me that perhaps I had grossly underestimated M.E.
I support Invest in M.E. because they understand
the true nature of M.E and help many sufferers of
this disease.
It was partly ignorance that killed my sister.
Yes you read that right, Sophia died from M.E.
She was 32 and her suffering and death were
largely preventable. Sophia‘s last wish was to help
others not go through what she did.
My sister was disbelieved by her doctors about the
true physical nature of her illness. She was accused
of attention seeking and having 'unresolved
issues' and she was treated as if her illness had its
roots in her mental health.
My mum who was my sister’s main carer was
accused of enabling Sophia’s illness for the simple
crime of believing that her daughter was
physically very ill. One of Sophia's doctors actually
wanted to section my mum. I wish I were
exaggerating but proof of all this is on
SophiandMe.org.uk.
Invest in ME is a charity that understands that M.E
is a physical disease and that M.E has been
categorised as a physical neurological disease by
the World Health Organisation since 1969. The way
M.E. is treated in this country is contrary to how a
physical, neurological disease should be treated.
In the UK, psychiatrists took charge of the care of
people with M.E., but this disease is not a mental
illness. It is like being treated by a dentist for a
broken leg. The wrong people are in charge of a
disease that they have no expertise in dealing
with.
Invest in ME (Charity Nr. 1114035)
Roisin Mirza is the sister of Sophia Mirza
and is a qualified nurse.
Sophia died from ME. Disbelieved by
those providing healthcare for her
condition, she was sectioned by
psychiatrists who neither understood her
condition nor seemingly cared to
analyse her symptoms in a medical
way. Sophia was “sectioned as a result
of exercising her right not to go into a
particular ME Clinic.
Despite the fact that she was bedbound,
she reported that she did not
receive even basic nursing care, where
her temperature, pulse and blood
pressure, were never taken. Sophia told
me that her bed was never made, that
she was never washed, her pressure
areas were never attended to and her
room and bathroom were not cleaned
From Tuesday 22nd November, Sophia
could not move an inch, neither could
she sleep.
On Friday 25th she died..”
- taken from Sophia’s story on the IiME
web site
Page 35/76
Sophia Mirza

Journal of IiME
Volume 3 Issue 1
www.investinme.org
Call to Action - Why I Support Invest in ME
(continued)
We don’t know how you
get/develop/contract M.E, and we don’t
know how to cure it and therefore we could
all be at risk from M.E.
So why are psychiatrists and the mental
health sector given free reign over M.E?
The simple answer is ‘kerching’ and
politics/power play. There is a lot of money at
stake for the treatment and research of this
disease. It is in certain group’s interests to
keep M.E treated as a mental illness. The
Government is advised by psychiatrists about
the treatment of the disease of M.E and it is in
their interest to advocate mental health
treatments.
It is also in medical insurance companies’
financial interests to keep M.E treated as a
mental illness. If M.E funding were to go to the
physical health camp, it would have to battle
with the big boys such as Cancer and Heart
Disease for funding. In the mental health
camp there is far less competition.
The ring of ‘kerching’ is louder than the cry of
truth at the moment. However the truth will
out, and the sooner M.E is seen and treated
as a physical illness the better for everyone.
This is not just better for M.E patients and their
carers, it is better for everyone.
The false security of M.E getting labelled as
something in mental health is a dangerous
myth. You cannot catch a mental health
disease, but you can catch/develop a
physical disease.
Multiple Sclerosis and Parkinson’s disease
were considered mental illnesses before they
were wrestled out of mental health and put in
their rightful place in physical health
treatment. M.E is not the first and will probably
not be the last disease to be wrongly taken
by the mental health sector.
By supporting Invest in ME you are helping
liberate everyone. This (event) happened to
Sophia but it could happen to anyone of us.
My sister was condemned as mentally ill and
referred to a psychiatrist, even though no
mental health checks were done and it was
Invest in ME (Charity Nr. 1114035)
blatantly obvious to anyone that Sophia was
severely physically ill.
Sophia refused treatment at an ME clinic where
they treat ME patients with methods such as
GET (Graded Exercise) and CBT (Cognitive
Behaviour Therapy),. These treatments have
been proven to make M.E patients WORSE.
The clinics’ own statistics state that Graded
Exercise makes people with severe ME worse.
Sophia was given a ‘get well by a certain date
or be sectioned’ ultimatum which she failed to
get well for.
Sophia refused to go to the clinic because she
was just too ill to be able to risk treatments
which would probably cause her great harm.
This was a sane decision by Sophia. As a result
of making a sane decision an insane one was
taken by her doctors. Sophia was sectioned
into a mental health hospital and she never
recovered from this experience.
Sophia’s could not tolerate light, noise,
movement or smells. She lived the last few
years of her life in the dark, in bed and couldn’t
even read a book or listen to music. She was in
constant pain and if this were not bad enough,
she had to live under a blanket of fear and was
treated as if she were mentally ill, despite
overwhelming evidence to the contrary.
My sister’s post-mortem revealed the physical
evidence of M.E in her spinal column. It is a
shocking disgrace that Sophia had to die to be
believed.
I trained as a nurse through my sister’s illness
and I saw how M.E was viewed from the other
side. I never confided in anyone during my
nurse training and nurse working time about my
sister having M.E, because of the stigma
attached to this disease. I didn’t risk confiding
in people because when I had tried confiding
in people before, I was met with plastic
psychiatry about ‘perhaps she has unresolved
issues’.
If you got M.E from having ‘issues’ the whole
country would be down with it. There was also
the risk that a well meaning but ignorant
person would add fuel to the fire and go to the
Page 36/76

Journal of IiME
Volume 3 Issue 1
www.investinme.org
Call to Action - Why I Support Invest in ME
(continued)
authorities with their ‘concerns’. This practise is
encouraged by psychiatrists who use peoples
‘concerns’ to back up their mental health
treatment assault.
By supporting Invest in ME you are supporting
human rights. Sophia was stripped of her
human rights because of the mental health
label. By supporting and bringing to light the
truth about the disease of M.E you are helping
to save lives. You are helping prevent another
Sophia story happening.
By supporting Invest in ME you are saying
that M.E is a physical disease that needs to be
treated as such. This matters to those countless
M.E sufferers and their carers that you
understand they are genuinely physically ill.
There is no physical diagnostic test for ME at the
moment but how can there be a physical
marker test for ME if no research money is put
there?
This must change.
I will be going back to my old nursing school
and giving a talk about Sophia and her ME on
June 8th.
Ignorance of ME is producing much
unnecessary suffering.
We need as much help as possible to turn the
image of M.E around.
Racism is rightly taken very seriously, but what
about ’diseasism’ ? There is a stigma with M.E
that is similar to a sixteenth century witch hunt.
The accusation of being called mentally ill, is
similar to that of calling a woman a witch.
Treating someone as if they are mentally ill,
does not make that person mentally ill. How
can someone prove they are physically ill if the
doctors treating them do not believe their own
eyes and ears?
Even without a diagnostic test for M.E there are
still physical abnormalities that would show up
in a blood test and other basic health checks.
Many doctors are reluctant to physically test for
ME because the “experts’ ” advice that it
‘encourages aberrant illness beliefs’.
ME is not a belief, it is a fact.
Invest in ME (Charity Nr. 1114035)
Page 37/76
ME is as much a ’belief’ as I ’believe’ in gravity
and those psychiatrists ’believe’ they are
medically trained.
We need research into the physical nature of
M.E. We need people to be as aware of M.E as
they are of cancer.
You wouldn’t accuse a cancer patient of
imagining their illness because they had
unresolved issues.
Not many things in life are black and white, but
this is.
There is no ‘confusion /controversy’ about the
disease of ME except the confusion the 'expert'
psychiatrists have put there. By muddying the
waters , these psychiatrists, many of whom are
in the pockets of medical insurance
companies, are keeping M.E in their domain.
Chronic Fatigue Syndrome (CFS) and M.E are
being lumped together as the same disease
but they are not the same. M.E. is a physical
neurological disease, and CFS is am umbrella
term for any disease with fatigue in.
Chronic Fatigue is classified by W.H.O as a
mental health illness, but M.E is classified as a
physical, neurological disease.
One can see how the lack of clarity starts to
happen.
A small powerful band of psychiatrists have, for
years, clouded and complicated the
understanding of the disease of M.E, not just in
the consciousness of ordinary people, but in
the minds of doctors, psychiatrists and the
Government, by talking about ME and
fatiguing syndromes in the same breath.
People are still suffering unnecessarily from the
physical disease of ME and from the unspoken
accusation that it is 'all in their mind' because
of a small group of doctors’ greed for money
and position. People are living under fear of
being sectioned because they ’believe’ they
are physically ill with M.E. Carers of those with
ME have a much higher rate of being accused
of Munchhausen’s By Proxy .

Journal of IiME
Volume 3 Issue 1
www.investinme.org
Call to Action - Why I Support Invest in ME
(continued)
It is scandalous that the very vulnerable ME
patients are not only not helped, but actually
discriminated against because they have M.E.
Please help us change this.
Anyone can get M.E. Sophia was half Pakistani
and half Irish. This is not just a white person’s
disease. We are all at risk and we need urgent
research and treatment into the
physical nature of this disease.
Behind the closed doors of courts, children are
being torn away from their parents. These
parents are silenced by these same courts.
Tell the mental health sector to 'Get your hands
off M.E' and put M.E back in its rightful place,
back where it belongs, back to where the
W.H.O. put it in 1969, back in the field of
physical disease.
ME STORY
I now live on DLA and have to use a
wheelchair. I spent years being told I
had
depression, I was attention-seeking,
difficult, lazy.
I tired too hard to do the things other
children/ young adults did and failed. I
felt hopeless and helpless many times.
However I refused to give up fighting.
THREE years ago after another round of
arguing with doctors and neurologists
and being told by a neuro psyche I was
not genuinely ill my GP
found missing notes from the 1980s -
notes that had been missing for over 20
years.
There in black and white were
handwritten notes than indeed I had
attended the doctors who had noted
possible encephalitis.
- Lynn
Invest in ME (Charity Nr. 1114035)
I have been diagnosed with CFS they
(the NHS) will not have ME in their
vocabulary.
Everything is a fight, to be heard, to be
listened to, just to be BELIEVED.
I wish with all my heart that I just was a
bit tired like people think, I would chop
off my arms to be just tired. My life is a
process of trying to get through the day
and perhaps I'll have a day where I'm
not so bad
- Maxine
Page 38/76
ME FACTS
In 2003, Byron Hyde, medical adviser
on ME/CFS to the Canadian
Government, pointed out that
“ME in adults is associated with
measurable changes in the central
nervous system and autonomic
function and injury to the
cardiovascular, endocrine and other
organs and systems.
The patient with the diagnosis of
ME/CFS is chronically and potentially
seriously ill.
These ME/CFS patients require a total
investigation
and essentially a total body mapping
to understand the pathophysiology of
their illness and to discover what other
physicians may have missed.
A patient with ME is a patient whose
primary disease is central nervous
system change, and this is measurable.
The belief that ME/CFS is a
psychological illness is the error of our
time”.
(The Complexities of Diagnosis. Byron
Hyde. In: Handbook of Chronic Fatigue
ME STORY

Journal of IiME
Volume 3 Issue 1
www.investinme.org
DIETARY SUPPLEMENT HEALTHY CURB FOR REDUCING WEIGHT,
GIRTH, BODY MASS, APPETITE AND FATIGUE WHILE IMPROVING
BLOOD LIPID VALUES WITH NTFactor LIPID REPLACEMENT THERAPY
Garth L. Nicolson, PhD, Rita Ellithrope, MD and Robert Settineri, MS
The Institute for Molecular Medicine, Huntington Beach, CA 92647
The Tustin Longevity Center, Tustin, CA 92780
Sierra Productions, Irvine, CA 92606
ABSTRACT
Often Chronic Fatigue Syndrome (CFS) patients have
weight issues, and weight reduction regimens can
increase fatigue. Therefore, we initiated a weight loss
clinical trial using an all natural oral supplement
mixture containing an FDA-approved amaylase
inhibitor plus NTFactorTM, which is known to safely
reduce fatigue in aged subjects,1 chronic fatigue2 and
CFS.3 The objective was to see if subjects could safely
lose weight without increasing appetite and fatigue
and without changing eating or exercise patterns or
using drugs, herbs or caffeine. A 2-month open label
clinical trial was initiated with 30 patients who used an
oral mixture (Healthy CurbTM) of amaylase inhibitor
(500 mg white kidney bean extract) plus 500 mg of
NTFactorTM 30 min before each meal. Weight and
measurements were taken weekly, appetite was
assessed4 and fatigue was determined using the Piper
Fatigue Scale.5 Sixty-three percent of the participants
lost an average of 6 pounds along with 2.5 and 1.5
inch reductions in waist and hip circumference,
respectively, and the entire group of participants lost
an average of 3 pounds with average reductions of
1.5 and 1 inch waist and hip circumference,
respectively. Participants experienced gradual and
consistent weight loss along with waist and hip, body
mass index (BMI) and basal metabolic rate (BMR)
reductions during the entire trial. There was a 44%
reduction in overall hunger with reduced cravings for
sweets; therefore, notable appetite suppression
occurred. Using the Piper Fatigue Scale the entire test
group showed an average of 23% decrease in overall
fatigue. Blood lipid profiles generally improved,
suggesting improved cardiovascular health, and no
adverse effects were noted clinically or found in blood
chemistries.
Conclusions: The vast majority of the subjects in this
trial lost weight, showed decreased waist and hip
measurements and overall body mass. Their overall
fatigue was reduced, and they experienced marked
appetite suppression. The product was completely
safe and void of any side effects and was extremely
Invest in ME (Charity Nr. 1114035)
Professor Garth Nicolson
The Institute for Molecular
Medicine,
P.O. Box 9355,
S. Laguna Beach,
California 92652.
Tel: 949-715-7958;
Email: gnicolson@immed.org;
Website: www.immed.org
ME RESEARCH
“Many studies have found that the
immune system appears to be in a
state of chronic activation (and)
genes that control the activation of
the immune system are
abnormally expressed in patients with
this illness. A number of studies
have shown that there probably
are abnormalities of energy
metabolism in patients with this
illness”.
Professor Anthony Komaroff of the
Harvard Medical School
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Journal of IiME
Volume 3 Issue 1
www.investinme.org
DIETARY SUPPLEMENT HEALTHY CURB FOR REDUCING WEIGHT, GIRTH,
BODY MASS, APPETITE AND FATIGUE WHILE IMPROVING BLOOD LIPID
VALUES WITH NTFactor LIPID REPLACEMENT THERAPY
(continued)
well tolerated. HealthyCurb appears to be a
safe and effective means for CFS patients to
manage weight without changes in eating or
exercise patterns.
INTRODUCTION
Being overweight or obese can present health
issues and may also lead to serious chronic
illnesses. Dieting is difficult because dieters are
unable to endure the commitment required to
achieve their weight loss goals. One of the
most common complaints of dieters is the
constant feeling of hunger associated with
reducing calorie intake. Another complaint
dieters experience is the lack of energy due to
decreased caloric consumption. Nutritional
Therapeutic, Inc. has developed a safe, allnatural
food-based supplement (Healthy
CurbTM) that has been reported to reduce
appetite, increase energy levels, reduce
fatigue, block starch uptake and help with
weight management. The supplement
contains NTFactorTM , which has been shown to
reduce fatigue and repair mitochondrial
membranes.2,3 This study was designed to
explore the degree of appetite suppression,
the degree of energy level, fatigue reduction,
changes in specific blood markers for
metabolic health and the amount of weight
loss and reduction in waist and hip
measurements in a 60 day trial.
PROCEDURES
A two-month open label clinical trial was
initiated with 30 patients, ages 18 and older,
who used an all-natural oral mixture (Healthy
CurbTM, http://www.healthycurb.com) of FDAapproved
amaylase inhibitor (2 tablets
containing 500 mg white kidney bean extract
plus 500 mg of NTFactorTM) 30 min before each
meal. All subjects filled out a medical intake
form at Tustin Longevity Center. The medical
staff determined if participants were qualified
to enter the study based on medical history.
Chronic fatigue was an important entry criteria.
Weight, waist and hip measurements were
taken weekly, appetite was assessed by the
procedures of Arumugam et al.,4 and fatigue
Invest in ME (Charity Nr. 1114035)
was determined using the Piper Fatigue
Scale.5
Blood samples were taken at the beginning
of the study and at the end of the study.
Weight, body composition and
measurements were taken every two weeks
until the end of the study.
During this two-month study the NIH
guidelines for alcohol consumption were
followed: “Moderate drinking is one drink a
day for women or anyone over 65, and two
drinks a day for men under 65.”
RESULTS
Weight and Girth Reduction: The entire
group of participants lost an average of 3
pounds (Fig. 1a) with average reductions of
1.5 and 1 inches in hip and waist
circumference, respectively (Figs. 2a, 3a).
Sixty-three percent of the participants
(responder group) lost an average of 6
pounds (Fig. 1b) along with 2.5 and 1.5
inches reduction in hip and waist
circumference, respectively (Figs. 2b, 3b),
and participants experienced gradual and
consistent weight loss along with waist and
hip reductions during the entire trial.
ME STORY
I had suffered neurological symptoms for
a number of years but by 2003 they had
reached the point where I couldn't
ignore them any longer.
I decided to go to the doctor. By great
good fortune I took the first appointment
available and saw a GP new to the
practice.
I told her my story, we discussed ME and
she said she neither believed nor
disbelieved in the illness.
She was more interested in the patient
than a 'tag', she said.
But for the first time since my diagnosis I
had found a doctor who actually
listened to me.
- Jim
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Journal of IiME
Volume 3 Issue 1
www.investinme.org
Letter from America
By Maary Schwweitzer
The Current Situation in the U.S.
These are exciting times for patients in the
United States.
The presidential election represented a
significant shift in policy towards medicine,
treatment, research, and the plight of the
neglected.
In December, the Obama-Biden transition
team asked for community meetings to
discuss health care issues. A small group of us
“met” online and produced a report on
ME/CFS.
One community report from every state was
chosen for the White House’s new website for
Health Reform – and ours represents my state
of Delaware:
http://healthreform.gov/communityreports/d
elaware/delaware_19711.html.
It has already been read by Senators,
Congressmen, and members of the executive
branch.
The research group IACFS/ME met in Reno,
Nevada, in March, with most sessions devoted
to international biomedical research.
The new Whittemore-Peterson Institute in Reno
is already bearing fruit using the tools of
molecular medicine.
Dr. Nancy Klimas noted how exciting to see
such diverse research presented in a
cooperative, not competitive, fashion.
April 27, the U.S. CDC held a hasty
stakeholders’ meeting on their new 5-year
plan for CFS and “fatiguing illnesses.”
The Obama administration was, we believe,
unprepared for the vehement response.
Person after person testified to the
consequences of having been rendered
invisible by CDC’s adoption of the name and
concept of “chronic fatigue syndrome.”
Invest in ME (Charity Nr. 1114035)
Mary M. Schweitzer, Ph.D.
Mary Schweitzer from Delaware,
USA, was a tenured professor of
history before being disabled with ME
in 1994.
Mary has been an active and very
passionate advocate for people with
ME for several years writing articles
and taking part in the CFSAC (Chronic
Fatigue Syndrome Advisory Committee)
meetings to allow the patient's voice
being heard.
For four hours patients, advocates, and a few
physician/researchers called for the
immediate end of the current CDC program
on CFS.
Consensus is building towards the goal of
subgroups identified through objective
biomedical testing, funding for treatment,
and the establishment of Centers of
Excellence as we have for cancer.
If CDC cannot help, then we want them to
step out of the way.
Written comments on the CDC’s 5-year plan
can be sent from inside or outside the U.S.
through June 30. See the website
http://www.cdc.gov/cfs/meetings/2009_04.ht
m.
On May 27 and 28, the Chronic Fatigue
Syndrome Advisory Committee (CFSAC)
within Health and Human Services will hold its
first meeting under the Obama administration.
We are all hopeful that the entire approach
to our disease will change, particularly
regarding NIH and CDC.
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Journal of IiME
Volume 3 Issue 1
www.investinme.org
Letter from America
The Current Situation in the U.S.
The agenda includes both the CDC’s 5-year
plan and the particular plight of children and
adolescents with CFS.
Unfortunately, just as parents have had to
fight to keep their sick children from being
sectioned in the UK, in the U.S. we are seeing
too many cases where a child has been
forcibly removed from his/her parents and
isolated in foster care.
Patients both at home and abroad are
responding to the current plight of 16-year-old
Ryan Baldwin, who has a CFS diagnosis.
After being diagnosed with a related heart
condition last year, Ryan qualified for social
security payments for disabled children.
In January Ryan was suddenly taken away to
a foster home. His parents were charged with
“factitious illness by proxy” and denied
access, even by phone.
Testimony from noted specialist Paul Cheney
proved that the heart condition vacated a
diagnosis of “factitious illness.” The authorities
then responded by asking the mother to
plead to “dependency” [upon her child
remaining ill].
She refused, and the court recessed for a
month with Ryan still in foster care.
We are grateful for a letter sent to the
governor of North Carolina by Invest in ME.
Anyone interested in helping with the case
can find information here:
http://cfsknowledgecenter.ning.com/profiles/
blogs/free-ryan-baldwin
The situation in the United States remains
desperate for many patients, but there is also
hope.
If emphasis turns from the psychosocial
to the biomedical, within five years
diagnosable subsets can be identified and
begin treatment.
We thank Invest in ME for its work in achieving
that goal.
Invest in ME (Charity Nr. 1114035)
The European ME Alliance
(EMEA)
Its aims are to -
• Establish correct recognition of
myalgic encephalomyelitis as an
organic illness requiring biomedical
research to treat and cure
• Establish correct diagnosis of patients
• Establish specialised biomedical
centres for
education/treatment/cures
NICE COMMENT
For (NICE’s Professor Peter) Littlejohns and his
superiors to ignore completely how damaging
this case (the Judicial Review of NICE
guidelines ofr ME) has been to NICE is myopic
in the extreme.
“The only thing worse than being blind is
having sight but no vision.” (Helen Keller)
How many more patients will need to
challenge decisions by NICE before the
government is forced to act and overhaul the
management and the objectives of this
organisation?
An organisation that purports to be
“committed to promoting equality, eliminating
unlawful discrimination, and actively
considering the implications of its guidance for
human rights” and yet is taken to court by the
same patients for whom it claims to promote
good healthcare – this is an organisation that
deserves to be overhauled.
from –
http://www.investinme.org/IIME%20Campaigni
ng-NICE-Whats-Next.htm
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Journal of IiME
Volume 3 Issue 1
www.investinme.org
It was fourteen years ago, on 18th February
1993, that Dr Paul Cheney, Professor of
Medicine at Capital University USA, Medical
Director of the Cheney Clinic in North
Carolina, and one of the world’s leading
exponents on ME/CFS, testified before the
FDA Scientific Advisory Committee in a
testimony that has become one of the most
quoted in history:
“I have evaluated over 2,500 cases (of ME).
At best, it is a prolonged post-viral syndrome
with slow recovery.
At worst, it is a nightmare of increasing
disability with both physical and
neurocognitive components.
The worst cases have both an MS-like and an
AIDS-like clinical appearance.
We have lost five cases in the last six months.
The most difficult thing to treat is the severe
pain. Half have abnormal MRI scans. 80%
have abnormal SPECT scans. 95% have
abnormal cognitive-evoked EEG brain maps.
Most have abnormal neurological
examination. 40% have impaired cutaneous
skin test responses to multiple antigens. Most
have evidence of T-cell activation. 80% have
evidence of an up-regulated 2-5A antiviral
pathway. 80% are unable to work or attend
school. We admit regularly to hospital with an
inability to care for self”.
Invest in ME (Charity Nr. 1114035)
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Journal of IiME
Volume 3 Issue 1
www.investinme.org
Epidemics of ME
EPIDEMICS of ME
Epidemics are associated with ME.
A Review of The Clinical Syndrome Variously
Called Benign Myalgic Encephalomyelitis,
Iceland Disease and Epidemic
Neuromyasthenia by E D Acheson (American
Journal of Medicine, 1959)
by Dr J Gordon Parish
Many of the findings described in the landmark
Acheson 1959 paper are very much relevant to
our understanding of ME today. The disease
was initially thought to resemble poliomyelitis
until distinguishing features occurred; no patient
developed the paralysis and muscle wasting
seen in poliomyelitis which is a disease of the
spinal cord.
Naldrett White, a Canadian neurologist, and
Robert Burtch, an American family physician,
described an epidemic in 1950 in Upper New
York State in the USA in an area close to the
Canadian border. They thought that muscles
were directly involved during the initial
infection. Accompanying a mildly elevated
temperature to 99–100 ºF (37.2–37.8 ºC) in
nearly every patient, there was pain and
tenderness in various muscles sometimes with
increased skin sensitivity over the affected
areas making contact with clothes or bedding
very unpleasant. In contrast to hypersensitivity,
difficulty in moving limbs and numbness with
diminished skin sensation on clinical testing
suggested peripheral nerve involvement.
Where there was weakness on using a hand
and sensory symptoms, examination revealed
an ulnar nerve disorder.
Nerve roots were sometimes involved in the legs
and were tender to pressure. This was
associated with dragging of the legs on walking
or foot drop. Another feature was
lymphadenopathy in some patients. Enlarged
tender anterior neck or axillary lymph glands
are mentioned.
Examination of the blood and cerebrospinal
fluid showed only minor abnormalities in two
patients. White and Burtch thought that they
might be dealing with an infection affecting
Invest in ME (Charity Nr. 1114035)
From the Incline village episode to the
Royal Free. Yet little is discussed about
these. In the 4th International ME/CFS
Conference Professor Harald Nyland will
discuss the recent epidemic associated
with Giardia in Norway. Yet this isn’t new.
It seems relevant to recall this review by
Dr Gordon Parrish of an article by E D
Acheson in the American Journal of
Medicine
muscle. The standard test for muscle damage
at that time was 24 hour urinary creatine
excretion, and this was found to be raised in
the 13 patients who were tested with a
tendency for the urinary creatine to fall to
normal levels as the patients recovered.
The creatine phosphokinase enzyme test for
muscle damage was not available at that
time. Subsequently, it was found to be normal
or only slightly elevated in ME suggesting that
the disturbance is different from that found in
other muscle diseases.
The illness had a striking resemblance to the
disease described by Sigurdsson and others in
Iceland during the winter of 1948–1949, and
hence the name Iceland Disease was
suggested for the illness.
In a leading article published anonymously in
the Lancet in May 1956, Acheson reviewed
eight similar outbreaks and suggested a title
Benign Myalgic Encephalomyelitis for the new
clinical entity based on the presumed
underlying pathology.
He considered the disease to be "benign"
compared with other epidemic infections of
the nervous system seen in various types of
encephalitis and in poliomyelitis due to the
absence of patients dying. However, "benign"
was later deleted from the title, leading to the
abbreviation to ME, because in some cases
the severity and duration of the disability
resulting from the disease was far from being
benign. He mentioned that hepatitis and
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Journal of IiME
Volume 3 Issue 1
www.investinme.org
E EPPIIDDEEMMIICCSS ooff MMEE ((ccoonnttiinnuueedd))
enlargement of the spleen might occur in
addition to lymph gland involvement
indicating the reticuloendothelial system
participated in the clinical picture in some of
the epidemics.
Alexis Shelokov and colleagues investigated
an outbreak involving 50 student nurses and
their tutors participating in residential courses
at a psychiatric hospital near Washington DC,
USA in 1953.
Half the patients had muscle weakness and
poliomyelitis was suspected then eliminated.
No other cause for the muscle weakness was
found. All patients had features of a
generalised illness similar to that described in
patients with Iceland Disease. After the initial
illness there was a subacute phase lasting
several months consisting of episodes of
feeling unwell and further muscle weakness.
Donald Henderson and Alexis Shelokov
reviewed 23 similar epidemics in 1959. They
found that the affected muscles were tender
either diffusely or in focal discrete areas,
which felt "oedematous, doughy or rubbery in
consistence". They introduced the term
Epidemic Neuromyasthenia, linking
neurasthenia with myasthenia to describe the
clinical picture. The term neurasthenia is
unfortunate as it implies a disturbance of
behaviour, which can follow an infection or
be the result of stress, in the form of irritability
and an inability to take exercise without
excessive fatigue. Similar disturbances
including crying spells without provocation
are also seen during the convalescence of
patients who have had strokes or head
injuries. The association of similar behavioural
disturbances with brain cell disorders such as
cranial nerve palsies and hemiparesis with
extensor plantar response is mentioned by
Henderson and Shelokov (1959) as an
occasional finding in some epidemics.
The association is clearly illustrated by Melvin
Ramsay in a serious of sporadic cases
admitted to an infectious diseases
department of a local hospital from the
population of North West London in 1955 and
1956. Rather than labelling the illness
neuromyasthenia a slight change to
Invest in ME (Charity Nr. 1114035)
neuronomyasthenia indicating a disease of
nerve cells (or neurones) and muscle cells
with muscle weakness might be more
appropriate. Neurologists prefer to limit the
term myasthenia to myasthenia gravis, a
disorder of the neuromuscular junction which
may present as a severe type of muscle
weakness. In patients with Myalgic
Encephalomyelitis/Neuronomyasthenia
(ME/NM), "myasthenia mitis" has been used to
describe a milder form of myasthenia in which
muscle weakness develops during normal
daily activities. Clinical tests were
subsequently developed, which measure the
declining muscle performance with activity
and the slow recovery of muscle afterwards.
In 1998 this delayed recovery of muscle
function after a fatiguing isometric exercise
test was confirmed in 1999 by Lorna Paul and
colleagues.
MERGE has funded research which has
revealed abnormalities in the function of
blood vessels and blood cells. Abnormalities
of blood vessels have been described in
these epidemics of ME/NM. Infectious
material was transferred from patients to
monkeys during an epidemic in Adelaide,
Australia in 1949–1950. The monkeys became
ill and post-mortem examinations were
carried out a month later. The only
abnormalities discovered by Pellew and Miles
(1955) were minute red spots along the
course of the sciatic nerves.
Under the microscope the red spots
contained localised collections of
inflammatory cells, which had also infiltrated
the area where the nerve roots come out of
the spinal cord. The red colour of the spots
was due to leakage of red blood cells.
ME/NM is very rarely fatal so that a postmortem
study showing similar haemorrhages
in humans is unique.
However, during the North of England
epidemic in 1955 Andrew Wallis described the
findings in a patient in her fifties, who
developed the characteristic febrile illness
leaving her debilitated and emotional.
During the next fifteen months she continued
to run a low grade fever with continued
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Journal of IiME
Volume 3 Issue 1
www.investinme.org
E EPPIIDDEEMMIICCSS ooff MMEE ((ccoonnttiinnuueedd))
mental deterioration before she died. The
post-mortem revealed numerous small
haemorrhages around blood vessels in the
cerebral cortex extending into the midbrain,
which were considered to be the
cause of her death.
These abnormalities may be found when
patients die as the result of severe chronic
alcoholism. This was not a factor in her case;
she had had a febrile illness. Vasculitis
involving the skin was recorded during
outbreaks in Cumberland, Durham and
North West London in 1955. A
maculopapular rash may appear during the
return of features of the initial illness such as
flu-like symptoms and enlargement of lymph
glands and liver. This skin overlying areas of
localised muscle weakness may be affected
at the time of these attacks.
In conclusion, Iceland Disease and ME/NM is
a muscle/brain disorder, which occurs as
clusters of cases in families, in institutions
such as hospitals or schools, in districts as far
apart as the northern townships in Iceland
and Adelaide in Australia or sporadically. It
is an infectious disease with an incubation
period of 5 to 8 days. Acheson in 1959 used
the expression "in a greater or lesser degree"
to describe "the symptoms and signs of
damage to the brain and spinal cord" in this
disease. This expression can also be applied
to the febrile illness and muscle involvement.
Many patients recover and return to normal
activities in weeks or months, while others
have relapses with reactivation of features
of the initial illness and further damage to
new areas of the brain or muscles.
In extreme cases deterioration may lead to
death. Muscle weakness has been
measured in a few patients. After activity
the recovery of muscle power is prolonged
to an extent not recorded in any other
disease. The association between these
findings in muscle and vascular
abnormalities in blood vessels and blood
components needs exploring. For research
purposes ME/NM patients with these
physical signs should not be coupled with
Invest in ME (Charity Nr. 1114035)
patients whose main illness is chronic fatigue
on exertion and who do not have these
signs.
References
- Acheson ED. The clinical syndrome
variously called Benign Myalgic
Enchephalomyelitis, Iceland Disease and
Epidemic Neuromyasthenia. Am J Med
1959; 26: 569-595.
- Henderson DA, ShelokovA. Epidemic
Neuromyasthenia – Clinical Syndrome. N
Engl 1959; 260: 757-764, 814-818.
- Leading Article A new clinical entity?
Lancet 1956; 1: 789-790. Written by ED
Acheson, introducing the term Benign
Myalgic Encephalomyelitis.
- Paul L, Wood L, Behan WMH, Maclaren
WM. Demonstration of delayed recovery
from fatiguing exercise in chronic fatigue
syndrome. European J Neurol 1999; 6: 6369.
-
Pellew RA, Miles JA. Further investigations
on a Disease resembling Poliomyelitis
seen in Adelaide. Med J Aust 1955; 42:
480-482
- Ramsay AM. Encephalomyelitis in North
West London. An endemic infection
simulating poliomyelitis and hysteria.
Lancet 1957; 2: 1196-1200. Description of
10 cases illustrating the association of
behavioural disorders (neurasthenia) with
brain disorders (cranial nerve palsies).
- Shelokov A, Habel K, Verder E, Welsh W.
Epidemic Neuromyasthenia. An
outbreak of poliomyelitis-like illness in
student nurses. N Engl J Med 1957; 257:
345-355. The Chestnut Lodge Epidemic,
Washington, USA in 1953.
- Sigurdsson B, Sigurjonsson J, Sigurdsson
JHJ, Thorkelsson J, Gudmundsson KR. A
disease epidemic in Iceland simulating
Poliomyelitis. Am J Hyg 1950; 52: 222-238.
- Wallis AL. An investigation into an
unusual illness seen in Epidemic and
Sporadic Form in a General Practice in
Cumberland in 1955 and subsequent
years.
- White DN, Burtch RB. Iceland Disease – a
new infection simulating Acute Anterior
Poliomyelitis. Neurology 1954; 4: 506-516.
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Journal of IiME
Volume 3 Issue 1
www.investinme.org
WHAT I WANT FROM an ME SERVICE
This article appeared in our Journal and on IiME’s web site in August 2007 and was written by Linda
Crowhurst, a severely affected person with ME, As we plan to discuss the ME Clinic at the IiME
Conference it was felt appropriate to republish this.
I need :
• Acknowledgement that ME is a WHO (ICD 10 -
G93.3)defined neurological disease. An
appropriate biomedical definition.
• Appropriate diagnostic criteria that
acknowledge the wide number of specific
physical symptoms.
• A biomedical clinician who can recognise the
symptoms of ME and their impact. and make
appropriate recommendations, based on
current physical research.
• Appropriate biomedical tests and scans that
prove that I have a physical illness and
illuminate what is going wrong in my body.
• An appropriate biomedical assessment that
will provide a medically-informed report
about my illness and disability.
• Acknowledgement of severe disability so that
support can be given to claim benefits and
grants etc, to enable true entitlement.
• Careful testing and monitoring before any
drugs are prescribed.
• Advice based on awareness to ensure safe
practice and safe treatments regarding how
to deal with other medical conditions and
illnesses that might arise.
• The neurological symptoms to be explored ,
prioritised and validated.
• Access by phone for specific symptom
management / backup.
• Home visits from a biomedical clinician.
• A service that is actively educating other
clinicians and paramedical staff regarding
the true physical nature and impact of this
disease.
• The opportunity to choose to participate in
Invest in ME (Charity Nr. 1114035)
physical research so that people who have
severe ME can be reflected in any research
evidence compiled.
• A service that is particularly aware of the
severity of my symptoms and the high level of
post-exertional malaise and post-exertional
fatigue I experience and can accommodate
them; so that I can be seen and given proper
ongoing support.
• The name "ME" to be used, as opposed to
"CFS".
What I do NOT want from an ME Service
• A focus upon "fatigue".
• A "therapy"-led service
• To be included with undefined Chronic
Fatigue illnesses and states.
• A psychosocial model of care.
• To be offered CBT and GET, as these are both
dangerous and unsuitable for people with ME.
• To be patronised by medical professionals
who do not believe that I have a physical
disease .
• To be downgraded and treated as if my very
real and severe neurological symptoms, such
as paralysis, spasms, parasthesia and pain
are insignificant or psychiatric in origin.
• To be offered psychiatric - originated
management techniques , charading as
treatment for this physical illness.
• To be described as "tired".
• Pretending to meet the needs of people with
ME but actually working to a psychiatric
paradigm.
• Any service based upon the Fukuda or Oxford
criteria.
Page 55/76

Journal of IiME
Volume 3 Issue 1
www.investinme.org
The 4tthh Invest in ME
International ME/CFS
Conference 2009
Emeritus Professor of Medicinal
Chemistry the University of Sunderland
Professor Hooper has published some 50
papers in peer-reviewed journals in the
field of medicinal chemistry. He has
By Professor Malcolm Hooper
Conference Introduction
Invest in ME conferences have rightly become
renowned for their high quality and eminent
international speakers who have successively
presented the most up to date biomedical
information about this perplexing and devastating
illness.
ME is a complex chronic multi-system illness, CMI.
Myalgic encephalomyelitis, muscle pain with
inflammation of the brain and spinal cord, is a
term that is both clinically meaningful and
accurately descriptive of the nature of the illness.
It has been known since 1934.
The name, first coined in 1956 by Donald Acheson
who subsequently became Chief Medical Officer,
was included, for the first time, in the World Health
Organisation’s International Classification of
Disease in 1969 chapter G.93.3, neurological
conditions.
To this day it is still so classified and the UK
Government has stated that it accepts this
classification although in every other way is acting
and legislating to the contrary.
The introduction in 1988 of the alternative
description, Chronic Fatigue Syndrome, CFS,
describes only a symptom and has led to
confusion, deception and obfuscation resulting in
Invest in ME (Charity Nr. 1114035)
served on committees of the Council for
National Academic Awards (CNAA), the
World Health Organisation (WHO) and
the Science and Engineering Research
Council (SERC).
He is a member of a number of learned
bodies, including the Royal Chemical
Society, the British Pharmacological
Society and the Society for Medicines
Research, where he has served on the
committee for 12 years and served as
Chairman for 2 years.
He was appointed Chief Scientific
Advisor to the Gulf Veterans Association
(GVA) and accepted by the Ministry of
Defence (MoD) as their nominee on the
Independent Panel established to
consider the possible interactions
between Vaccines and NAPS tablets. His
involvement with the GVA brought
contact with Chronic Fatigue
Syndrome/Myalgic Encephalomyelitis
(ME/CFS) and related disorders. Gulf War
Illness/Syndrome (GWI/S) has much in
common with ME/CFS.
He worked with the Autism Research Unit
(ARU) at the University of Sunderland for
over 20 years, leading to involvement in
biochemical studies to offer help,
support and treatment for people with
autism. He served on the General Synod
of the Church of England from 1970 to
1980 and he is a Christian Lay Leader,
Preacher and Teacher.
Page 56/76

Journal of IiME
Volume 3 Issue 1
www.investinme.org
The 4th Invest in ME International ME/CFS
Conference 2009 (continued)
the sometimes acrimonious and bitter debates
about the nature of the illness.
The imprecise word fatigue has been used by
some psychiatrists to label ME as a behavioural
and mental disorder. Such disorders are
classified under F.48.0 which includes chronic
fatigue and fatigue syndromes that are quite
distinct from neurological conditions.
Today the diagnosis, treatment and
management of ME are bedevilled by these
two conflicting understandings of the illness
leaving People with ME (PWME) frequently
marooned, mistreated and misunderstood
both medically and socially.
C CPPDD AAcc ccrr eeddii tteedd
The most severely disabled patients have
suffered the greatest neglect. Exciting new
possibilities for treatment that can change the
lives of patients offer new hope for their future.
M Maannaaggeemmeenntt,, TTrreeaattmmeennttss aanndd tthhee
L Laatteesstt AAddvvaanncceess iinn RReesseeaarrcchh iinnttoo
M MEE//CCFFSS
O Onnee BBii rrddccaaggee WWaa llkk ,, WWeess ttmmii nnss ttee rr ,, LLoonnddoonn
It is particularly apt that this 4th Conference is
specially concerned with the severely disabled
who have born the brunt of the present
obdurate, heartless and official views of ME
that treat sick patients and their carers so
cruelly.
It is a joy to welcome the speakers for this
conference who come from the USA, Norway,
Belgium as well as the UK.
The Whittemore-Peterson Institute, WPI, offers
both challenge and hope to the world of ME
with the “can do” energy and commitment so
Invest in ME (Charity Nr. 1114035)
The third arm of the Institute involves research
studies that address the nature of the illness and
lay the foundations for new understanding and
treatments of ME.
Judy Mikovits, Research Director of the WPI,
presents her insights in to the diagnosis of the
difficult and most complex ME cases. Diagnosis is
the key to clinical treatment and definitions of
ME are crucial for managing and effectively
treating individual patients.
An institute that brings patients, clinicians and
research workers together can provide a
springboard for major advances in the ME. The
WPI provides such a working paradigm and is a
challenge to every country where ME is a major
health issue.
John Chia has done great service by providing
clear evidence of the role of enteroviruses in ME.
Their role first identified by earlier workers in the
field including, John Richardson, Irving Spurr,
Byron Hyde and others, has been confirmed and
extended by John’s work.
His story makes it essential that the
microbiological services that have been
dismantled in this country must be re-established
to support clinical need and research into
Page 57/76
typical of the American response to any
daunting situation.
This Institute provides a working model of how to
engage with ME and the growing number of
complex CMIs that are emerging in today’s
world.
Annette Whittemore has provided the resources
to bring the Institute into being and has an
inspiring story to tell of how love, care and sheer
‘guts’ has realised a model for the rest of the
world to follow.
Dan Peterson is the Medical Director of the WPI
and has long wrestled with ME and provided
hope, expert clinical care and understanding for
numerous patients and carers for PWME.

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The 4th Invest in ME International ME/CFS
Conference 2009 (continued)
effective treatments for enteroviral infections.
Pooled human immunoglobulins are still effective
in the very early stages of the illness, the first 6
months, but if this window of opportunity is
missed then the illness may develop into a more
chronic condition with serious consequences for
the patient and the need for long drawn out and
expensive therapy
Garth Nicolson has, at great personal cost,
engaged with various CMIs and in the early days
recognised the strong similarities between
ME/CFS and Gulf War Syndrome.
The recent Binn’s report on Gulf War Illness clearly
identifies the importance of chemical exposures
in this CMI although vaccine exposures may still
play an important role.
Chemical and biological exposures leading to
neurodegenerative and neurobehavioural
changes need to be better understood.
Garth has provided effective antibiotic
treatments for ME that follow some intracellular
microbial infection, for example with
mycoplasma organisms.
Previous Invest in ME conferences have
emphasised the inadequacies of the current
Fukuda/CDC definition of ME/CFS and the
importance of sub-groups. Clarity is greatly
needed in this area.
Norway, as a result of powerful and persistent
campaigns by ME suffers and activists led by
Ellen Piro, has changed official attitudes towards
ME by showing the effects of vaccines in
provoking the illness which may also arise from
natural infections.
Barbara Baumgarten heads a newly established
ME-centre that provides correct diagnosis,
treatment and management of ME emphasising
once again the need for accurate diagnosis as
the sine qua non for effective therapy for PWME.
Will this new centre be the beginnings of a
European WPI?
The seminal book by Hillary Johnson makes clear
the need to consider the epidemiology of ME
which is important for prompt action with regard
to the illness. Although intracellular organisms,
including rickettsia, chlamydia, borellia are wellknown
to give rise to ME the epidemiology of
Invest in ME (Charity Nr. 1114035)
Giardiasis, an extracellular parasite can teach
us lessons that are valuable in engaging with
ME.
Harald Nyland will make these interesting links
in his presentation.
Kenny de Meirleir has championed patient
needs and treatment in Europe and also
contributed to the Canadian definition of
ME/CFS. He has written perceptively about the
disruption of essential immunological
mechanisms in this illness by micro-organisms,
heavy metals and other environmental
chemicals. Case studies are the key to building
up clinical understanding of the complexity of
ME and its various manifestations that so
perplex those newly encountering with this
illness. We will learn much from his experiences.
Jonathan Kerr has carried out ground breaking
studies in the genetics of ME especially in the
most severely affected patients. This new field
provides deeper understanding of the multisystem
nature of the illness and shows how it
can relate to other CMIs. The use of genetic
analysis to identify clinical phenotypes for
diagnosis and treatment will enable accurate
sub-grouping of patients and targeted
treatments to be developed and applied to
this needy group of patients.
Jonathan’s genetic studies show how a
multiplicity of environmental insults can impinge
upon a smaller number of key biochemical
pathways and give rise to a multiplicity of
symptoms – this is great gain and supports the
experiences of many sick patients.
Basant Puri, also at great cost, has used
advanced neuro-imaging techniques to
investigate the structural and chemical
changes in the brain associated with ME and
devised useful treatments that specifically
address these changes.
The multi-system nature of ME requires a
conference Chairman who is familiar with the
illness in all its manifestations. Jonathan Brostoff
is such a person and has a vast experience in
all the complexities of immunology and
conducts research into allergy and
environmental health issues.
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The 4th Invest in ME International ME/CFS
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We are in for a splendid conference which
provides real hope for all who suffer from ME
and all those who care for them.
The medical and health community and, not
least, medical and research administrators
need to hear these stories and be prepared
to learn from them, support biomedical
research, and thereby serve the needs of
sick patients.
In the UK we need an institute comparable to
the WPI. When will the cry of sick patients and
their carers be heeded and action taken to
make effective treatment(s) available?
When will money be allocated for biomedical
research that addresses the real nature of this
illness.
Much money has been devoted to support a
model of ME that belittles patients, labels
them with a diagnosis of a behavioural and
mental disorder, and offers pacing (largely
commonsense to people with any chronic
illness), cognitive behavioural therapy, CBT,
which even its strongest advocate state is
“not remotely curative”, and of doubtful
efficacy, graded exercise therapy, GET,
which makes many patients more ill
(confirmed by biological studies), coupled
with antidepressants which may provoke
chemical sensitivities and are not necessary
since many patients are not depressed.
This conference once again provides solid
biomedical evidence which cannot continue
to be ignored by health services increasingly
wedded to an ideological, anti-clinical, and
anti-scientific view of an illness that is now
better understood and for which effective
treatments following careful diagnosis are
available.
Enjoy it!
Spread the message, challenge the
bureaucrats, in Government, the NHS, and
MRC and reclaim this field of medicine for
both present and future patients.
Malcolm Hooper
May 2009
Invest in ME (Charity Nr. 1114035)
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OSLER’S WEB
To welcome Hillary Johnson to London we
would like to highlight the later version of
Osler’s Web. This has been updated by Hillary.
From the review by Maryann Spurgin at
http://www.cfids-cab.org/MESA/reviews4.html
“..the most provocative portion of Johnson's
discussion concerns the federal research
establishment's attempt to manufacture a
mental disorder out of a physical
symptomatology. In meticulous detail,
Johnson shows how bias in the choice of
patients, value-laden selection of CFSrelated
data and prejudicial allocation of
research funds permitted government
researchers to conclude that CFS was a
psychiatric condition, or rather, something
more akin to a behavioral problem. If
Johnson is correct, then the government's
conclusion is a classic illustration of the
Thomas Szasz thesis: The concept of mental
illness is often a political tool with which
society dismisses its inconvenient members.”
Ms Spurgin states that one of Osler's
Web's strong points is its illustration of a
propaganda system at work where studies
citing negative findings in CFS were readily
published, whilst studies reporting positive
physiological findings were turned down.

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PROFILES of PRESENTERS at the INVEST in
ME INTERNATIONAL ME/CFS CONFERENCE
C Coonnffeerreennccee CChhaaii rr ::
P Prrooffeessssoorr JJoonnaatthhaann BBrrooss ttooff ff MMAA DDMM DDSScc((MMeedd)) FFRRCCPP FFRRCCPPaatthh FF IIBBiiooll
Jonathan Brostoff is Senior Research Fellow and Professor Emeritus of Allergy and Environmental
Health at Kings College, London. He was the Foundation Professor of Allergy and Environmental
Health and Director of the Centre for Allergy Research at University College London. Whilst at
University College Hospital he was Physician in charge of the Allergy Clinic.
He is recognized as a leading international authority on food allergy and intolerance.
Professor Brostoff was involved in one of the few, and much-quoted Spect scan studies of ME
patients [Brainstem perfusion is impaired in patients with chronic fatigue syndrome. Costa DC,
Tannock C and Brostoff J. Quarterly Journal of Medicine 1995:88:767 773].
A Annnneett ttee WWhhii tt tteemmoorree
Founder and President of the Whittemore Peterson Institute for
Neuroimmune Diseases, Reno, Nevada, USA.
Annette Whittemore graduated from the University of Nevada with
a BS Ed in Elementary and Special Education. Teaching children
who had neuro-cognitive deficits, like those found in autism, ADD,
and learning disabilities, provided her with a unique experience to
later use in her pursuit of answers to her daughter's serious illness.
Annette is the parent of a young adult who was severely affected by CFS and HHV-6. She and
her husband are business owners and philanthropists in Reno and Sparks. Annette Whittemore is
President and Co-founder of the foundation and became active in starting the HHV-6
foundation.
She started the foundation with Kristin Loomis from California after a brief meeting in Incline, NV.
with Dr. Daniel Peterson, a leading clinical researcher in CFS and HHV-6.
When her daughter became ill with a chronic neuroimmune disease, Annette began to seek
appropriate medical care. Annette found that few doctors understood the reasons for her
daughter's continuing physical decline. For this reason, Annette has committed her time and
resources to bringing attention to the serious nature of neuroimmune diseases and change her
community in a positive way. She began this important mission in 1994 by supporting a Think Tank
on ME/CFS, led by Dr. Daniel Peterson of Incline Village. In 2004 she and another patient
advocate began a medical foundation to support research to find biomarkers of disease and
treatments for patients impacted by the HHV-6A virus.
In order to provide solutions for patients and bring new doctors into this field of medicine,
Annette, legislators, and others supported a bill to build a biomedical research center at the
University of Nevada, Reno with an Institute for Neuro-Immune disease and the Nevada Cancer
Institute. Annette founded the Whittemore-Peterson Institute for Neuroimmune Diseases which is
being built on the medical campus with its mission to serve those with complex neuro-immune
diseases such as ME/CFS, viral induced central nervous system dysfunction and fibromyalgia.
In addition, Annette and Harvey have contributed over one million dollars and pledged another
four million dollars in support of the building and programming to bring this project to fruition.
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As the Founder and President, Annette supports the basic and clinical research programs,
recruitment of physicians and support personnel, while also leading fundraising activities.
Researchers at the University of Nevada Medical School have also become collaborators on
projects that are vital to our understanding of the immune deficits seen in these patients.
The Nevada Business Journal recently honored Annette and her husband Harvey as Health Care
Heroes for their personal commitment to this Institute and its mission. Other community activities
include current positions on the Governing Board of the Davidson Institute and the Community
Board of Pack Paws (thanks to the HHV-6 Foundation and the WPI web site for this information).
P Prrooffeessssoorr GGaarr tthh NNiiccooll ssoonn PPhhDD
The Institute for Molecular Medicine,
P.O. Box 9355, S. Laguna Beach, California 92652.
Tel: 949-715-7958;
Email: gnicolson@immed.org; Website: www.immed.org
Professor Garth Nicolson Phd (Biochemistry/Cell Biology),
President, Chief Scientific Officer and Research Professor, The Institute for Molecular Medicine;
Conjoint Professor, Faculty of Science and Technology, University of Newcastle, Newcastle,
Australia; Professor of Integrative Medicine, Capital University of Integrative Medicine,
Washington DC.
Professor Nicolson has been studying the role of infections in chronic illnesses such as Gulf War
Syndrome, Chronic Fatigue Syndrome, Autoimmune and Degenerative Diseases for many
years. He is also an extinguished cancer researcher and has many publications to his name,
including 3 Current Content Citation Classics.
The Institute for Molecular Medicine is a research institute and its mission is to contribute to the
understanding of and the prevention and cure of catastrophic human chronic diseases, such
as autoimmune diseases, fatigue illnesses, rheumatic diseases, cancer, AIDS, and infectious
and genetic diseases. This will be accomplished through innovative basic and translational
research programs.
P Prreesseenn ttaatt iioonn:: SSiimmii llaarr iinnffeecctt iioonnss ffoouunndd iinn MMEE//CCFFSS aanndd
N Neeuurrooddeeggeenneerraatt iivvee aanndd NNeeuurroobbeehhaavviioorraall DDii sseeaasseess ..
Garth L. Nicolson1, Nancy L. Nicolson1, Jorg Haier2
1The Institute for Molecular Medicine, Huntington Beach, California,
2Department of Surgery, University Hospital, Munster, Germany
Objective: The majority of neurodegenerative diseases, fatiguing illnesses and neurobehavioral
disease patients have chronic infections.1,2 Therefore, we examined the presence of certain
co-infections in the blood of patients with Autism Spectrum Disorders (ASD) and compared
these to ME/CFS patients.
Methods: North American ME/CFS and ASD patients were examined for various infections by
isolation of leukocyte blood fractions and forensic polymerase chain reaction (PCR) to
determine various infections.3,4
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P Prrooffeessssoorr HHaarraalldd NNyyllaanndd MMDD,, PPhhDD
Institute of Clinical Medicine, Department of Neurology, Haukeland University Hospital, 5021
Bergen, Norway
On 20 July 2006 Professor Nyland was knighted by the King of Norway for his services for MS
research and treatment of MS patients. Since the 1970s he has built up a large multidisciplinary
research team at Haukeland University Hospital which has worked with immunological diseases
in the brain and other parts of the nervous system. Professor Nyland has published over 100
scientific papers in international publications, either as the main author or as a senior co author.
He has also taught neurology students for more than 20 years. Thanks to Professor Nyland’s
considerable input the Neurology Department at Haukeland University Hospital is at present a
national centre of excellence for MS in Norway. Dr Nyland graduated in 1968 and took his
medical PhD in 1982. He has also been strongly involved with ME patients for more than 10 years
and during this time he has examined over 1500 patients with suspected ME.
P Prreesseenn ttaatt iioonn::
Epidemics & ME: Lessons from the Giardia epidemic in Norway
Background
In 2004 a few thousand people contracted a gastrointestinal infection due to consumption of
contaminated public drinking water (1). According to Nygard et al. (2), approximately 48,000
people were exposed to the contaminated tap water during the outbreak. People affected had
been drinking tap water from the public waterworks supplying the inner city of Bergen, a coastal
city of western Norway, during the outbreak.
Leaking sewage pipes combined with insufficient water treatment were the likely causes of the
epidemic (1). The outbreak probably began in August and peaked in early October (2). A total
of 1300 laboratory-confirmed cases of Giardia duodenalis were reported (1). In addition one
could expect a number of asymptomatic carriers as well (3). It took about six to eight weeks
before the medical community and local health authorities acknowledged the epidemic and
identified the parasite, G. lamblia, as the cause of the gastrointestinal infection (4). One reason
for the late detection of the cause is probably that G. lamblia is non-endemic in Norway and
therefore not normally tested for (2).
The people infected were mostly women and younger people (2, 4) who had been drinking
larger amounts of tap water, often more than five glasses per day (2). The municipality of Bergen
city accepted responsibility for the insufficient quality of the water supply and their insurance
carrier is expected to pay compensation. Most cases are still being arbitrated, and some may
end up in court.
G. lamblia is one of the most common causes of protozoally-induced diarrhoea in humans
globally (1, 5), but in Norway before 2005, this infection was mainly associated with people
travelling to “exotic” places, as more than 90 % of yearly confirmed cases are imported by
foreign travellers (5). This outbreak of giardiasis is the largest waterborne outbreak in recent time
(5), and the first reported giardiasis outbreak of epidemic proportion in Norway (6).
An outbreak of this size is unusual in the Nordic countries, and even in Europe. Information from
the Norwegian Prescription Database revealed that probably more than 2,500 cases were
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treated for giardiasis, likely associated with this epidemic (2).
Most of the affected patients responded well to standard treatment with antibiotics, although
for some only one cure was not sufficient to clear the parasite from the body (4). After treatment
some returned to their general practitioners because they experienced recurring symptoms (5).
Following the Bergen giardiasis epidemic a few hundred developed post-infectious irritable
bowel syndrome [PI-IBS] (8), and many still experienced abdominal symptoms and prolonged
fatigue two years after the initial infection (9).
Around 2005 and 2006, severely fatigued patients started to be referred to a neurologist
specialising in chronic fatigue syndrome (CFS)/myalgic encephalomyelitis (ME) for further
investigation. The majority of the fatigued patients subsequently participated in an educational
programme in the fall of 2007, focusing on following aspects: post-infectious prolonged fatigue
(disease knowledge); physical activity; psychological aspects accompanying severe illness;
nutrition; legal entitlements administered by the Norwegian Labour and Welfare Administration,
as well as future plans for a rehabilitation programme aimed to facilitate recovery and return to
work or education.
After a thorough examination, 58 persons fulfilling the 1994 Fukuda et al. (10) criteria for chronic
fatigue syndrome were consecutively enrolled in a prospective multidisciplinary research project
(11). Data show that among this subgroup of severely fatigued persons, some had become
acutely fatigued (25%), some after a few weeks (14.3%), and some more gradually over several
months (60.7%). The multidisciplinary research project’s main objectives are: 1) Present the
clinical findings for the group of patients with post-infectious fatigue syndrome and to determine
symptomatic and functional status during a 5-year follow-up; 2) Explore and describe the
patients’ own experience of living with this condition and being in a rehabilitation process. The
research study being presented in this paper is focusing on the human aspects of living with
giardiasis.
References
1. Eikebrokk B, Gjerstad KO, Hindal S, Johanson G, Rostum J, Rytter E (2006). Giardia utbruddet i
Bergen. Sluttrapport fra det eksterne evalueringsutvalget. (Report in Norwegian)
http://www.sintef.com/
2. Nygard K, Schimmer B, Sobstad O, Walde A, Tveit I, Langeland N, Hausken T & Aavitsland P. A
large community outbreak of waterborne giardiasis - delayed detection in a non-endemic
urban area. BMC Public Health, 2006;6:141 doi:10.1186/1471-2458-6-141
3. Rortveit G & Wensaas K-A. En moderne epidemi. [A modern epidemic] Tidsskr Nor
Laegeforen, 2004;124(24):3178.
4. Steen K & Damsgaard E. Giardiaepidemien i 2004 og Bergen Legevakt. [The Giardia
epidemic in 2004 and out-of-hours service in Bergen] Tidsskr Nor Laegeforen, 2007;127(2):1879.
5.
Wensaas KA, Langeland N, Rortveit G. Prevalence of recurring symptoms after infection with
Giardia lamblia in a non-endemic area. Scand J Prim Health Care, Dec 2008;12:1-6.
6. Nygard K. Giardiasis – et undervurdert problem i Norge. [Giardiasis--an underestimated
problem in Norway?] Tidsskr Nor Laegeforen, 2007;127(2):155.
7. Wensaas K-A, Langeland N, Rortveit G. Avdekking av giardiasisutbruddet i Bergen 2004.
[Uncovering the giardiasis-outbreak in Bergen 2004] Tidsskr Nor Laegeforen,
2007;127(17):2222-5.
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Additional links for Dr Kerr:
Jonathan Kerr, Seven genomic subtypes of Chronic Fatigue Syndrome / Myalgic
Encephalomyelitis (CFS/ME): a detailed analysis of gene networks and clinical
phenotypes. J Clin Pathol. 2007 Dec 5. ub ahead of print] PMID: 18057078 [PubMed - as
supplied by publisher]
D Drr .. BBaa rr bbaa rr aa BBaauummggaa rr tt eenn MMDD
Project leader , ME/CFS-center, Oslo University Hospital, Ullevål
Dr Barbara Baumgarten was born in Hamburg, Germany, and moved
to Norway in 1980. She studied medicine at the University of Oslo and
from 1992-93 she worked at a hospital in internal medicine and
surgery. From 1993 she has been working in General Practice, with a
two year assignment at a nursing home.
Since 1996 she has had her own practice and has been seeing patients with ME since 1997.
From April 2006 she has been working one day a week as a GP at the department for
infectious diseases, Ullevål University Hospital, Oslo. Her work there was to look at the need of
specialized medical services for ME-patients. That has resulted in a new ME-clinic. Since
August 2008 her main job at Ullevål University Hospital has been leader for the new MEcentre,
which was officially opened on December 11th 2008.
The ME Centre in Oslo is unique in that patients have been closely involved in its formation. Dr
Baumgarten has given many lectures about ME for GP’s, at hospitals and for the Norwegian
ME Association. She is a board member at the Oslo branch of the Norwegian Medical
Association.
P Prreesseennttaatt iioonn DDrr .. BBaauummggaarr tteenn::
S Seerrvviicceess ffoorr ccoorr rreecctt ddiiaaggnnooss ii ss
a anndd MMaannaaggeemmeenntt //TT rreeaattmmeenntt ooff MMEE
Thanks to the ME-patient organizations in Norway, Norwegian politicians have become
aware of the problems ME patients face, both concerning diagnosis and treatment of their
condition. Some years ago there were only a few doctors who knew enough about Post
infectious fatigue syndrome, as it was most commonly called then, to set the diagnosis.
One of the doctors who would recognize the condition was Dr. Oddbjørn Brubakk who was
head of the department for infectious diseases at Ullevål University Hospital in Oslo. Two
patients had approached him in 2003 and asked if it was possible to start a coping course for
patients with ME since there was little other treatment to offer them. A group including the
patient representatives and professionals from the medical division and the Patient
education center at Ullevaal started working on a concept for a course that has been
running twice a year since 2004. Therefore, when political awareness around ME was growing
Ullevaal University Hospital was asked by the Eastern Norway Regional Health Authority to
have a closer look at the needs of that patient group. Since 2006 I have been working on a
concept for a ME-clinic and last year we got funded by the South-Eastern Norway Regional
Health Authority to start the clinic as a project. We have today an out-patient clinic where
patients can come to get diagnosed, and where they can get help in coping with ME by a
multi professional team that includes an occupational therapist, a physiotherapist, a dietitian
and a social worker. Patients get help to learn energy economizing, relaxation techniques,
dietary advice and advice with their problems with the social security system. When working
on the concept I became aware that the permanently bedbound patients wouldn’t be able
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to come to our clinic. So I introduced the concept of an ambulatory team that could go home
to people helping to get the correct diagnosis and offering them the same advice with up to
five visits by two from the team each time. The limitation is that we must be able to do the visit in
one day including transportation, so we cover only eastern Norway. These services have just
started and now the South-Eastern Norway Regional Health Authority have asked Oslo University
Hospital, Ullevaal (three University hospitals in Oslo joined by January 1st 2009) to investigate the
possibility of starting an in-patient service for severe ME-sufferers, which would cover the whole
country. The ward would provide the possibility for careful examination to rule out all other
conditions that might explain the condition and give those who can profit from
treatment/coaching that possibility.
Our biggest concern at this time is that patients with very severe ME will be too ill to be moved to
the ward and might become worse by physical examinations.
The report is handed over to the authority by April 30th and we hope to have an answer by mid
June.
P Prrooffeessssoorr KKeennnnyy DDee MMeeii rr lleeii rr MMDD PPhhDD
Dr. De Meirleir is a world renowned researcher and is professor of
Physiology and Internal Medicine at Free University of Brussels in
Belgium. He is co-editor of Chronic Fatigue Syndrome: A Biological
Approach, and reviewer for more than 10 other medical journals.
Dr. De Meirleir was one of four international experts on the panel
that developed the Canadian Consensus Document for ME/CFS.
He assesses/treats 3,000 to 4,000 ME/CFS patients annually. Professor Kenny L. De Meirleir, MD
received his medical degree at Vrije Universiteit Brussel, Magna cum laude. His research activities
in Chronic Fatigue date back to 1990. His other research activities in exercise physiology,
metabolism and endocrinology have led to the Solvay Prize and the NATO research award. He is
director of the Himmunitas Foundation Brussels and Professor at the Vrije Universiteit Brussel, as
well as consultant in the Division of Cardiology and director of the cardiac rehabilitation
program at Vrijie Universiteit Brussel.
P Prreesseennttaatt iioonn PPrrooffeessssssoorr DDee MMeeii rr lleeii rr ::
R Reesseeaarrcchh oonn EEeexxtt rreemmeellyy DDeebbii ll ii ttaatteedd MM..EE .. PPaatt iieenntt ss RReevveeaall ss tthhee TT rruuee
N Naattuurree ooff tthhee DDii ssoorrddeerr
Kenny De Meirleir(1), Chris Roelant(2), Marc Fremont(2), Kristine Metzger(2), Henry Butt(3)
(1) Vrije Universiteit Brussel & HIMMUNITAS foundation, Brussels, Belgium
(2) Protea Biopharma, Brussels, Belgium
(3) Bioscreen & Bio 21, University of Melbourne, Melbourne, Australia
In this study we compared totally bedridden patients (Karnofski score 20-30) with less ill ME
patients (Karnofski score 60-70), family controls, contact controls and non-contact controls. EBV,
HHV6 and Borna virus titers were not different in the three groups. Plasma LPS distinguished the
groups, with the highest values in the bedridden patients. LPS is a strong activator of the immune
system and high plasma concentrations suggest a hyperpermeable gut. There are many possible
causes for this, but a lack of ‘local’ energy production is one of them. In a separate study (In
Vivo, in press) we observed intestinal overgrowth of Gram positive D/L lactate producing
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bacteria which are also known to produce H2S in presence of certain heavy metals as a survival
defense mechanism. We therefore hypothesized that the urine of the bedridden ME patients
would contain more H2S derived metabolites than the less ill and the controls. Using a proprietary
simple colorimetric urine test this hypothesis was confirmed.
In the extremely ill, urine added to the yellow color reagent immediately turns dark blue,
whereas in the less ill the reaction is slower and in the controls no reaction occurs.
Being a potent neurotoxin, H2S induces photophobia, intolerance to noise, mitochondrial
dysfunction by inhibition of cytochrome oxidase, depresses the cellular immune system and
induces neutropenia and low numbers of CD8+ lymphocytes. Its effects, at least in part explain
the clinical condition of the severely disabled ME patients.
Furthermore bacterial H2S induces increased ROS production by the liver and retaining of heavy
metals, particularly mercury, in the body. Mercury is also neurotoxic, induces apoptosis and
interferes with the aerobic metabolism. Chronic increased production of H2S by intestinal
bacteria leads to build-up of mercury in the body as proven by a Zn DTPA/DMPS challenge test.
In about 20% of the ME patients (the most severely ill) we observed using a special luminescence
technique the formation of proteins with aberrant conformation which interfere with the energy
metabolism.
In conclusion, ME is a disorder which is caused by increased endogenous H2S production. H2S
initiates a chain of events in the body, with more and more negative effects on the aerobic
metabolism and depression of the immune system leading to higher rates of infections and
reactivation of endogenous viruses. In the most severe cases of the disease proteins with
aberrant conformation may develop which put the patients in a total energy depleted state.
Examples of other papers from Professor De Meirleir include –
Lower frequency of IL-17F sequence variant (His161Arg) in chronic fatigue syndrome patients.
Metzger K, Frémont M, Roelant C, De Meirleir K. Biochem Biophys Res Commun. 2008 Nov
7;376(1):231-3. Epub 2008 Sep 5. PMID: 18774769 [PubMed - indexed for MEDLINE]
Unravelling intracellular immune dysfunctions in chronic fatigue syndrome: interactions between
protein kinase R activity, RNase L cleavage and elastase activity, and their clinical relevance.
Meeus M, Nijs J, McGregor N, Meeusen R, De Schutter G, Truijen S, Frémont M, Van Hoof E, De
Meirleir K. In Vivo. 2008 Jan-Feb;22(1):115-21. PMID: 18396793 [PubMed - indexed for MEDLINE]
Dr. Daniel Peterson MD
Daniel Peterson is a graduate Magna cum Laude, Phi Beta Kappa of
Carleton College in Northfield, Minnesota. He graduated from the
University of Rochester School of Medicine in Rochester, New York, in 1976.
Dr. Peterson served his internship and residency at the University of Utah
Medical Center from 1976-1979 and became a Diplomat of the American
Board of Internal Medicine in 1979.
He has been caring for patients with Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome
(ME/CFS), for two decades, and his clinical work is complimented by a strong commitment to
research as evidenced by his participation in more than 17 research studies, numerous drug trials
and his foresight to collect and maintain the world's single largest repository of ME/CFS patient
samples. Dr. Peterson was on the founding board of the IACFS. Among the numerous awards that
he has received, in 2007 he was awarded the prestigious Nelson Gantz Clinician Award.
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With over 25 years of medical practice, Dr Daniel L. Peterson has become a sought-after internist
for diagnosing difficult and complex medical cases. When several patients in Incline Village
became ill with symptoms that resembled persistent mononucleosis, Daniel Peterson was one of
the first physicians to recognize an outbreak of what is known as ME/Chronic Fatigue Syndrome
(ME/CFS). He became a pioneering physician and researcher in understanding the biological
characteristics and methods for diagnosing, managing and treating ME/CFS. He has also
performed major studies of Ampligen as a treatment for ME/CFS, and studying the possible role of
human herpes virus 6 (HHV-6) in CFS patients.
Dr Peterson is an affiliate of the Sierra Internal Medicine Associates in Incline Village, Nevada;
ME/CFS researcher and clinician; a board member of the American Association for Chronic
Fatigue Syndrome; and member of the International Chronic Fatigue Syndrome Study Group.
Dr Peterson was one of the two physicians who identified the original outbreak of CFS in Incline
Village, Nevada, in 1984. (thanks to the WPI web site for this information).
C Coonnffeerreennccee PPrreesseennttaatt iioonn ::
T Trreeaattmmeenntt RReeggiimmeess ffoorr tthhee MMooss tt
S Seevveerree CCaasseess
Chronic Fatigue Syndrome/ME is a worldwide problem with incidence of approximately
700 people per 100,000.
A subset of patients diagnosed with CFS/ME are severely affected with marked resultant disability
and reduced quality of life.
In addition to clinical symptoms, these patients can be assessed
through objective markers and further categorized by degree of disability and severity of illness. In
addition to functional studies, biological markers exist, they are useful in establishing baseline
values and used to follow treatment regimens.
It is important to thoroughly evaluate these patients in order to rule out comorbid conditions that
are also treatable and to establish subsets allowing targeted interventions and rehabilitation
strategies. A diagnostic algorithm has been developed to identify this group of patients and to
facilitate aggressive treatment strategy. Biological markers can include genetic studies for
predisposition to ME, extensive immunological profiling to document perturbations of B-cell and
T-cell function and gene expression arrays.
Additionally, platforms exist to look for pathogenetic mechanisms including viral arrays and
cytokine analysis. Neuroimaging can further determine objective markers of CNS dysfunction.
Functional studies employed include studies of VO2 max and neurocognitive testing. Generally,
these severely affected subsets of patients have been ill for prolonged period of time and have a
guarded prognosis. However, dramatic results have been reported with aggressive targeted
strategies. A team approach is required in order to provide necessary services including in-home
services, hospitalization, and aggressive management for orthostatic intolerance, cognitive
dysfunction, and immune perturbations.
Objective markers are followed throughout this process to gauge effectiveness of therapy and
axillary supportive services are instituted concomitantly to address issues of secondary mood
disorder, deconditioning, and psychosocial dysfunction related to chronic illness.
A center of excellence model is currently being developed to implement this broad approach to
the most severely disabled patients that include translational research from the laboratory to the
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D Drr JJoohhnn CChhiiaa MMDD
Dr Chia is an infectious disease specialist practicing in
Torrance, California, USA and has published research
recently (Chronic fatigue syndrome associated with chronic
enterovirus infection of the stomach) on the role of
enteroviruses in the aetiolgy of ME/CFS – an area which has
been implicated as one of the causes by a number of
studies. There are more than 70 different types of
enteroviruses that can affect the central nervous system,
heart and muscles, all of which is consistent with the
symptoms of ME/CFS. By analyzing samples of stomach tissue
from 165 patients with CFS,
Dr. Chia's team discovered that 82% of these individuals had high levels of enteroviruses in
their digestive systems. Dr Chia's research may result in the development of antiviral drugs to
treat the debilitating symptoms of ME/CFS.
C Coonnffeerreennccee PPrreesseennttaatt iioonn ff rroomm DDrr CChhiiaa::
D Diiaaggnnooss ii ss aanndd TT rreeaattmmeenntt ooff MMyyaallggiicc EEnncceepphhaalloommyyeell ii tt ii ss//CChhrroonn iicc
F Faatt iigguuee SSyynnddrroommee AAssssoocciiaatteedd wwii tthh CChhrroonniicc EEnntteerroovvii rruuss iinnffeecctt iioonn..
J Joohhnn CChhiiaa,, AAnnddrreeww CChhiiaa.. EEVV MMeedd RReesseeaarrcchh
ME/CFS is an elusive illness without a clear etiology and treatment. Emerging evidences
suggest that enteroviruses can persist in the tissues of ME/CFS patients and may be
responsible for the various symptoms. Enteroviruses are common causes of respiratory,
gastrointestinal and non-specific flu-like illnesses. Major epidemics of enterovirus infections
including but not limited to meningoencephalitis, myocarditis, pleurodynia, myositis and
hand-foot-mouth diseases have been well-documented in the past decades.
In some cases, acute enterovirus infections can cause CD8+ T lymphocytopenia predisposing
to reactivation of endogenous herpes viruses. Initial isolation of enteroviruses from patients
with acute infections followed by demonstration of persistent viral infection in tissues years
after the patients developed chronic symptoms lends support to the pathogenic role of
enteroviruses in ME/CFS.
Presumptive clinical diagnosis of chronic enterovirus infection requires a high index of
suspicion, familiarity with the protean manifestations of acute infections and understanding
of chronic viral persistence.
There is not yet a specific diagnostic test for ME/CFS. Significantly elevated neutralizing
antibody titer over time suggests persistent immunologic response to specific enterovirus(s)
infection in the tissues. Neutralizing antibody test for 11 of the most common non-polio
enteroviruses is performed by one U.S. reference laboratory.
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In contrast to other types of viremic infections, EV RNA levels in whole blood of ME/CFS
patients are extremely low, which likely explain the discrepancy of results reported from
different research laboratories over the past two decades.
Immunoperoxidase staining for viral protein in the stomach biopsies is more sensitive than the
neutralizing antibody test or EV RNA detection, and furthermore, demonstrates the antigens
in tissues where viruses are expected to replicate and persist based on the route of
transmission.
The finding of enteroviral RNA and growth of non-cytopathic viruses from the same tissues
support the validity of protein staining.
As enteroviruses have been largely forgotten since the eradication of poliomyelitis through
effective vaccination, there is no specific antiviral therapy for acute or chronic infections.
Pleconaril, an anti-capsid agent, showed limited benefit in 1/4 patients with ME/CFS
associated with chronic enterovirus infections.
Intravenous immunoglobulin, given monthly or every few months, can ameliorate
inflammatory symptoms in less than 1/3 of adult patients, but may be more effective in
pediatric patients. The combination of alpha and gamma interferon can induce short-term
remission in about 45% of ME/CFS patients with debilitating myalgia, but is quite expensive
and often poorly tolerated.
One of the Chinese herbs, oxymatrine, has beneficial effect in 52% of 300 ME/CFS patients,
but transient increase in symptoms are expected in most of the patients.
Cytokine gene expression study during therapy demonstrates an increase of IL12/Il10 ration in
7/7 responders but in 0/10 non-responders. A decrease of stainable enteroviral protein is
demonstrated in the stomach biopsies of three responders on oxymatrine therapy.
Previous evidence for enterovirus infection in ME/CFS from over a decade ago has been
confirmed and extended in recent studies. Development of antiviral therapy against
enteroviruses is paramount; and the importance of enteroviruses in ME/CFS can be realized
with a randomized, placebo-controlled antiviral drug trial.
Additional links for Dr Chia:
John Chia, Chronic fatigue syndrome is associated with chronic enterovirus infection of the
stomach. J Clin Pathol. 2008 Jan;61(1):43-8. Epub 2007 Sep 13. PMID: 17872383 [PubMed -
indexed for MEDLINE]
Enterovirus infection as a possible cause of pityriasis rosea: demonstration by
immunochemical staining. Chia JK, Shitabata P, Wu J, Chia AY. Arch Dermatol. 2006
ul;142(7):942-3. No abstract available. PMID: 16847226 [PubMed - indexed for MEDLINE]
Diverse etiologies for chronic fatigue syndrome. Chia JK, Chia A. Clin Infect Dis. 2003 Mar
1;36(5):671-2; author reply 672-3. No abstract available. PMID: 12594650 [PubMed - indexed
for MEDLINE]
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D Drr JJuuddyy MMiikkoovvii tt ss PPhhDD
Dr. Mikovits obtained her Ph.D. in Biochemistry and Molecular
Biology from George Washington University. Dr. Mikovits served as a
senior scientist at Biosource International, where she led the
development of proteomic assays for the Luminex platform that is
used extensively for cytokine activity assessment in therapy
development.
Dr. Mikovits spent more than 20 years at the National Cancer
Institute in Frederick MD during which time she received her PhD in
Biochemistry and Molecular Biology, investigating mechanisms by which retroviruses
dysregulate the delicate balance of cytokines in the immune response. This work led to the
discovery of the role aberrant DNA methylation plays in the pathogenesis of HIV. Later in her
career at the NCI, Dr. Mikovits directed the Lab of Antiviral Drug Mechanisms (LADM) a section
of the NCI's Screening Technologies Branch in the Developmental Therapeutics Program. The
LADM's mission was to identify, characterize and validate molecular targets and to develop
high-throughput cell-based, genomic and epigenomic screens for the development of novel
therapeutic agents for AIDS and AIDS-associated malignancies (Kaposi's sarcoma). Formally
trained as a cell biologist, molecular biologist and virologist, Dr. Mikovits has studied the
immune response to retroviruses and herpes viruses including HIV, SIV, HTLVI, HERV, HHV6 and
HHV8 with a special emphasis on virus host cell interactions in cells of the hematopoietic system
including hematopoietic stem cells (HSC).
Dr. Mikovits' commercial experience includes serving as a senior scientist and group leader at
Biosource International, where she led the development of proteomic assays for the Luminex
platform that is used extensively for cytokine activity assessment in therapy development.
She also served as Chief Scientific Officer and VP of Drug Discovery at Epigenx Biosciences,
where she led the development and commercialization of cell and array-based methylation
assays for drug discovery and diagnostic development.
She is Research Director at the Whittemore Peterson Nevada CFS centre for Neuro-Immune
disorders and has co-authored over 40 peer reviewed publications that address fundamental
issues of viral pathogenesis, hematopoiesis and cytokine iology. (thanks to the WPI web site for
this information).
C Coonnffeerreennccee PPrreesseennttaatt iioonn DDrr MMiikkoovvii tt ss ::
T Trraannss llaatt iioonnaall RReesseeaarrcchh TToowwaarrddss tthhee DDiiaaggnnooss ii ss ooff DDii ff ff iiccuull tt aanndd
C Coommpplleexx MMeeddiiccaall CCaasseess ooff MMEE//CCFFSS
The research program of the Whittemore Peterson Institute is unique in that it has taken a
systems biology approach to the study of CFS. This approach involves profiling a patient with
respect to genetics, immune system phenotype and function and expression of viruses. Both
research and clinical data are entered into a central database for correlation with clinical
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data. These data are then translated into diagnostic and treatment strategies that can be
personalized” for each patient. This model can be extended to each physician such that data
from individual cohorts or subgroups of patients can be entered into a fully secure/ international
national database that can be queried by physicians anywhere in the world giving each
physician tools with which to diagnose and treat patients with similar genetic, immune and
pathogen profiles. We used this strategy to study more than 100 difficult and complicated CFS
patients from a well-defined Nevada ME/CFS cohort resulting from outbreak of ME/CFS that
occurred between 1984 and 1987. Immune profiling reveals immune defects including in T, B
and NK cell compartments.
These abnormalities are suggestive of a persistent infection and predicative of the development
of lymphoma. Moreover using antibody microarrays to profile serum biomarkers in this cohort we
have developed a five-cytokine/chemokine signature that can identify CFS patients from
controls with 94% sensitivity and specificity. Viral microarray studies demonstrate persistent active
herpes viruses, enteroviruses, adenoviruses and parvoviruses. Genetic profiling revealed HLA
and killer immunoglobulin receptor (KIR) genotypes predictive of susceptible and protective
genotypes in this cohort. Taken together these data suggest that this systems biology strategy
can be developed diagnostically, for the development of serum biomarkers to stratify subgroups
of ME/CFS patients for appropriate anti-inflammatory, antimicrobial and antiviral therapeutics.
Additional links for Dr Mikovits: http://lib.bioinfo.pl/auth:Mikovits,J
Example of other work:
Epigenetic control during lymphoid development and immune responses:
aberrant regulation, viruses, and cancer. Muegge K, Young H, Ruscetti F, Mikovits J. Ann N Y
Acad Sci. 2003 Mar;983:55-70. Review.
PMID: 12724212 [PubMed - indexed for MEDLINE]
The Invest in ME
International ME/CFS Conferences
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